Acta Otolaryngol 2000; 120: 580 595

Nasal Airflow in Health and Disease

RONALD ECCLES
From the Common Cold Centre, Cardiff School of Biosciences, Cardiff Uni6ersity, Cardiff, UK

Eccles, R. Nasal airflow in health and disease. Acta Otolaryngol 2000; 120: 580 595.
This review examines our present understanding of the physiology, pathophysiology and pharmacology of nasal airflow.
The main aim of the review is to discuss the basic scientific and clinical knowledge that is essential for a proper
understanding of the usefulness of measurements of nasal airflow in the clinical practice of rhinology. The review
concludes with a discussion of the measurement of nasal airflow to assess the efficacy of surgery in the treatment of nasal
obstruction. Areas covered by the review include: influence of nasal blood vessels on nasal airflow; nasal valve and control
of nasal airflow; autonomic control of nasal airflow; normal nasal airflow; nasal cycle; central control of nasal airflow;
effect of changes in posture on nasal airflow; effect of exercise on nasal airflow; effect of hyperventilation and rebreathing
on nasal airflow; nasal airflow in animals; cerebral effects of nasal airflow; sensation of nasal airflow; sympathomimetics
and sympatholytics; histamine and antihistamines; bradykinin; and corticosteroids. Key words: nasal airflow, nasal cycle,
nasal surgery, nose, rhinomanometry.

INTRODUCTION
The nose acts as the entrance to the airway and has
multiple functions as a passageway for airflow, a
chemosensor, an air conditioner and as the first line
of defence against respiratory infection. In humans
and all mammals the nose is divided into two
anatomically distinct passageways, each with its own
separate blood supply and nerve pathways. In this
respect, the nose can be considered as two separate
organs which may operate, on occasions, quite
independently.
The importance of nasal airflow in relation to
olfaction was appreciated by physiologists in the 19th
century but, with the development of medicine and
rhinology, clinicians became more and more concerned with the respiratory functions of the nose. In
order to properly assess the respiratory function of
the nose some means of quantifying nasal airflow was
essential. The problem facing the rhinologist in the
19th century was nicely described by Kayser in 1895
(1) and his observations are so relevant to the present
day rhinologist concerned with evidence-based
medicine that they are worth quoting at length: Although in most cases it seems easy to determine a
complete occlusion of the nose during an examination, in many cases it is difficult to translate this
objective finding into an assessment as to whether the
narrowing of the nasal passages actually impairs the
respiratory function of the nose. It is therefore important to be able to perform a functional examination
of the nose, i.e. determine whether the flow of air
through a particular nose (e.g. that of the patient) is
normal. Only the demonstration of a functional insufficiency of the nose can give our therapeutic intervention greater accuracy, and only in this way can we
demonstrate any effects of this intervention in an
objective manner. After all, we measure the acuity of
the eye and the hearing ability of the ear.
2000 Taylor & Francis. ISSN 0001-6489

When Kayser made this statement the only method

available to assess nasal airflow was that introduced
by Zwaaardemaker of Utrecht, The Netherlands,
who used a cool mirror to measure the condensation
spots obtained from each nasal passage on expiration. This method only provided a measure of the
relative conductance of each nasal passage and could
not be used to quantify the nasal airflow. Kayser set
out to devise an objective method of quantifying
nasal airflow that could be used in the clinic to assess
the respiratory function of the nose and his report of
1895 is the start of scientific studies on nasal airflow.
Repeated measurements of nasal airflow in normal
healthy volunteers demonstrated that the conductance of the nose was variable and that the conductance of the separate nasal passages alternated over a
period of between half an hour and several hours.
Kayser reported that Even greater variations occur
when the air conductance of each nasal passage is
measured separately. In rhinopathology, it is a common experience that people who complain of nasal
occlusion due to chronic rhinitis say that sometimes it
is one side and at other times it is the opposite side
that is occluded.
Kayser is often quoted as being the first to describe
the so-called nasal cycle but in fact he never used
this term. However, his studies do report the spontaneous alternations in nasal airflow that are often
referred to as a nasal cycle, and he did explain these
changes in nasal airflow as being due to changes in
the amount of blood flowing through the cavernous
tissues of the nasal conchae.
I have quoted the work of Kayser in some detail as
an introduction to this review on nasal airflow because it is so relevant to the problems of present day
rhinology and much of todays research work on
nasal airflow is merely an extension of the research

Acta Otolaryngol 120

performed by Kayser over 100 years ago. The development of electrical pressure transducers, flow heads,
computers, rhinomanometry and acoustic rhinometry
has made it much easier to obtain nasal measurements; however, rhinologists are still unsure how to
quantify the respiratory function of the nose in terms
of airflow and have not progressed much further in
understanding the nature of the spontaneous changes
in airflow associated with the nasal cycle.
This review will examine our present understanding
of the physiology, pathophysiology and pharmacology of nasal airflow. This basic scientific and clinical
knowledge is essential for a proper understanding of
the usefulness of measurements of nasal airflow in the
clinical practice of rhinology. The review will conclude with a look at some developments in nasal
surgery, where the measurement of nasal airflow has
been used to assess the efficacy of surgery in the
treatment of nasal obstruction.
PHYSIOLOGY OF NASAL AIRFLOW
Influence of nasal blood 6essels on nasal airflow
The importance of the nasal blood vessels in the
control of nasal airflow was appreciated by Kayser
(1) who talks of the cavernous tissues of the nasal
conchae as being involved in the control of nasal
airflow. An American contemporary of Kayser,
Wright (2), described the histology of the human
nasal epithelium as containing large venous sinuses
with muscular walls.
The congestion and decongestion of the nasal
venous sinuses was directly observed by Burnham in
1941 (3) who studied the localized responses of the
cavernous tissue in response to localized application of ephedrine. Burnham described three separate
areas of the inferior turbinate and, by localized application of ephedrine, was able to obtain decongestant
responses which were limited to one area or the
other.
In 1932 Schaeffer described the venous sinuses as
the corpora cavernosa and compared the activity
of these nasal blood vessels with that of cavernous or
erectile tissue. Schaeffer described the corpora cavernosa of the nose as especially well developed over
the inferior nasal concha, the overhanging border of
the middle concha, and the adjacent parts of the
nasal septum and he also said that there is some
evidence that there is an alternating erectility of the
mucous membrane of the two nasal fossa. The role
of the nasal venous sinuses in the control of nasal
airflow is now well recognized and their ability to
swell and completely obstruct the nasal passage has
been reported (4, 5). The location of the nasal venous
sinuses at the anterior tip of the inferior turbinate

Nasal airflow in health and disease

581

and nasal septum is critical for the control of nasal

airflow and this area of the nose is often referred to
as the nasal valve.
Nasal 6al6e and control of nasal airflow
The narrowest point of the nasal passage determines
the nasal resistance to airflow and this area is referred
to as the nasal valve (57). However, there is some
dispute in the literature as to whether the nasal valve
lies in the nasal vestibule or more posteriorly within
the bony cavum of the nose. The anatomical and
physiological evidence indicates that the nasal valve
occurs at the entrance of the piriform aperture, with
the major site of nasal resistance just anterior to the
tip of the inferior turbinate (8).
The nasal airway resistance can be thought of as
consisting of three components: the nasal vestibule;
the nasal valve; and the turbinated nasal passage.
These three components are illustrated diagrammatically in Fig. 1. The compliant nasal vestibule is
stiffened by cartilage to which facial muscles such as
the alae nasi attach. During inspiration these muscles
contract and splint the vestibule to prevent collapse.
The change in airway resistance along the nasal
passage can be determined by passing a pressuresensing cannula carefully along the passage and de-

Fig. 1. Diagram of the nose. The compliant wall of the

nasal vestibule is supported by the alae nasi muscles. The
nasal valve is at the level of the anterior tip of the inferior
turbinate. The diagram illustrates the normal asymmetry of
nasal congestion, with one side of the nose congested due
to swelling of the venous sinuses in the nasal turbinates and
the other side open and decongested due to constriction of
the venous sinuses. The degree of congestion of the tip of
the inferior turbinate determines the dynamic cross-sectional area of the nasal valve area and nasal airway resistance.

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R. Eccles

termining the pressure flow relationships during

quiet breathing. Using this technique, it has been
demonstrated that the major site of nasal resistance
lies at the anterior end of the inferior turbinate within
the first few millimetres of the bony nasal cavity (5).
The nasal valve is not a fixed anatomical constriction of the airway but a dynamic valve. The nasal
airway resistance is determined by swelling and constriction of the venous sinuses of the inferior turbinate and nasal septum which can cause complete
obstruction of the nasal passage. The significance of
the erectile properties of the inferior turbinate has
been discussed by Haight and Cole (5), who found
that the anterior end of the turbinate could advance
by as much as 5 mm after application of histamine.
The anterior site of the major component of nasal
resistance at the level of the tip of the inferior turbinate has important surgical implications as it follows that treatments such as diathermy (9), aimed at
reducing the swelling of the inferior turbinate, will
have major effects on nasal resistance whereas minor
corrective surgery, such as trimming of septal spurs
posterior to the nasal valve region, will have little
effect on nasal resistance.
The turbinated region of the nasal passage has a
relatively large cross-sectional area compared to the
nasal valve area. In the normal nose the turbinated
area has only a minimal contribution to the airway
resistance of a nasal passage.
Autonomic control of nasal airflow
Observations by rhinologists during the 19th century
established that the human nasal epithelium was subject to phases of congestion and decongestion due to
the filling and emptying of a network of venous
sinuses. However, the experiments which established
the role of the autonomic nerves in controlling the
volume of these nasal blood vessels were performed
on various animal models in the 20th century.
The first studies on nasal vasomotor activity were
performed by Tschalussow in 1913 using the dog as a
model (10). The method used by Tschalussow consisted of forming an airtight nasal cavity by sealing
the nasopharynx with Vaseline-soaked swabs and
sealing a y-shaped cannula into the nostrils. The
cannula was connected to a sensitive tambour and
pressure changes within the nasal cavity were
recorded on a smoked drum and kymograph.
Tschalussow demonstrated that stimulation of the
cervical sympathetic nerve caused a marked vasoconstriction of nasal blood vessels and he also demonstrated the presence of vasodilator fibres in the
Vidian nerve (nerve of the pterygoid canal) which
were shown to relay in the sphenopalatine ganglion.

Acta Otolaryngol 120

Sternberg in 1925 (11) used the same method as

Tschalussow and demonstrated that section of the
vagosympathetic trunk in the dog caused nasal vasodilation. Sternberg concluded that this vasodilator
response was due to interruption of a constant sympathetic tone to the nasal blood vessels. This was an
important finding as it established that alternation of
sympathetic nervous activity to the nose could cause
congestion and decongestion of nasal blood vessels
and by implication an alternation in nasal airflow.
Subsequent studies on experimental animals have
confirmed that the major control over the filling of
the nasal venous sinuses is via sympathetic vasoconstrictor nerves and that the parasympathetic vasodilator fibres only have a limited effect on nasal blood
volume (1216).
In general the autonomic innervation of the nose
can be considered in terms of parasympathetic control of nasal secretion and sympathetic control of
nasal airflow. The preganglionic parasympathetic
nerves originate close to the salivatory nuclei of the
brainstem and follow the greater superficial petrosal
nerve and nerve of the pterygoid canal (17). The
parasympathetic fibres relay in the sphenopalatine
ganglion and are then distributed to the glands of the
nasal mucosa. Electrical stimulation of the parasympathetic nerves causes a profuse watery nasal secretion (18) and Vidian neurectomy has been used for
the treatment of profuse watery rhinorroeah (19).
The parasympathetic neurotransmitter is acetylcholine accompanied by vasoactive intestinal
polypeptide, which is a potent vasodilator (20).
Parasympathetic nerve stimulation causes a watery
nasal secretion which is rapidly cleared from the
nasal passages without any effect on nasal resistance.
However the thick viscous mucus and plasma exudate
associated with upper respiratory tract infection can
influence nasal resistance by temporarily blocking the
narrowed airway and this can complicate the measurement of nasal resistance.
The sympathetic nerves to the nose are controlled
from areas in the hypothalamus and vasomotor areas
of the brainstem (21, 22). The preganglionic sympathetic nerves originate from the thoracolumbar regions of the spinal cord, relay in the cervical ganglia
and are distributed to the glands and blood vessels of
the nose via the nerve of the pterygoid canal and
branches of the trigeminal nerve.
The venous sinuses of the nasal mucosa have a
dense adrenergic sympathetic innervation (23) and
electrical stimulation of the sympathetic nerves to the
nose causes a pronounced vasoconstriction and a
marked decrease in the volume of blood held in the
mucosa (16, 24, 25). Noradrenaline is the primary
sympathetic neurotransmitter (accompanied by neu-

Acta Otolaryngol 120

ropeptide Y) and both of these neurotransmitters are

potent vasoconstrictors (26).
Although it is generally accepted that the nasal
venous sinuses are involved in the regulation of
airflow and that the filling of the venous sinuses is
controlled by the sympathetic nerves, the mechanism
regulating the swelling of the veins is poorly understood. Cauna (27) described throttle or cushion veins
which may control the filling of the venous sinuses
but there is no information on how the autonomic
nerves may control these throttle veins. Wright (2)
and Burnham (28) suggested that the close apposition
of arteries and veins in the bony canals of the turbinates was significant, as arterial dilation would
cause compression of the venous plexus draining the
erectile venous sinuses and this would lead to swelling
of the venous sinuses. The idea that dilation of
arteries contained in the bony canals of the turbinates
causes both an increased filling of the venous sinuses
and also restricts the outflow from the venous sinuses
is a reasonable hypothesis to explain the nasal congestion associated with a reduction in sympathetic
tone.
Under normal conditions, there is a continuous
sympathetic vasoconstrictor tone to the nasal venous
sinuses and section or local anaesthesia of the cervical
sympathetic nerves which supply the nasal mucosa
causes Horners syndrome with ipsilateral nasal congestion and an increase in nasal resistance to airflow
(2932).
Normal nasal airflow
With a standard resting tidal volume of 0.5 l and a
respiratory rate of 12 breaths per minute the combined volume of inspiratory and expiratory air passing through the nose is : 12 l/min. On a
breath-by-breath basis one can plot the relationship
between pressure and flow as a sigmoid curve. The
pressureflow relationships are not linear because at
most flow rates above zero the airflow is not laminar
and is best described as a mixture of turbulent and
orifice flow (33). As both the pressure difference
across the nasal passages (from nasopharynx to nostril) and the airflow through the nasal passages fluctuate during the respiratory cycle most researchers
prefer to calculate the nasal resistance to airflow by
measuring the airflow at a fixed pressure differential.
Rhinomanometry is generally accepted as the standard technique of measuring nasal airway resistance
and assessing the patency of the nose. Recently there
has been an upsurge of interest in acoustic reflectance
or acoustic rhinometry as it is sometimes termed.
Acoustic rhinometry gives measures of the cross-sectional area and volume of a nasal passage whereas
rhinomanometry gives a functional measure of the

Nasal airflow in health and disease

583

pressureflow relationships during the respiratory cycle. There are many useful reviews on the techniques
of rhinomanometry (3436) and acoustic rhinometry
(3739) and the practical and theoretical aspects of
these measurements will not be discussed in the
present review.
In subjects free from signs of nasal disease mean
total resistance has been reported to be : 0.23 Pa
cm3 s, with a range of 0.150.39 Pa cm3 s, by Morris
et al. (40), to be : 0.26 Pa cm3 s by Syabbalo et al.
(41) and 0.21 Pa cm3 s by Havas et al. (42). Cole (43)
reported that normal total nasal resistance lay in the
range 0.150.30 Pa cm3 s. Vig and Zajak (44) reported that normal adult nasal resistance was B0.2
Pa cm3 s. As a routine screening procedure in our
laboratory we normally consider a total nasal resistance to airflow of 0.3 Pa cm3 s as an upper limit of
the normal range.
Nasal resistance is a maximum in the infant at
: 1.2 Pa cm3 s (45, 46), declines to the adult value at
around 1618 years of age and then shows only a
slow decline with increasing age (Syaballo et al.) (41).
In a study on healthy volunteers Vig and Zajak (44)
reported a relationship between age and nasal resistance, with resistance declining with increasing age
from 0.6 Pa cm3 s (age 512 years) to 0.29 Pa cm3 s
(age 1319 years) and 0.22 Pa cm3 s (age \ 20 years)
in males. The relationship between age and nasal
resistance was similar in females but in general nasal
resistance was lower in females than in males (44).
Unlike other respiratory parameters, such as vital
capacity etc., there is no real correlation in the adult
between total nasal resistance and sex or height (40)
although several authors have claimed to have shown
a weak correlation with height (42, 47) and a negative
correlation with age (41). The lack of correlation
between total nasal resistance and height may be
related to the instability of nasal resistance due to
spontaneous congestion and decongestion of nasal
venous sinuses. If the nose is decongested by exercise
or application of a topical decongestant then this
eliminates any physiological variation in resistance
and allows one to investigate the anatomical factors
influencing resistance. Studies by Broms (48) have
provided a table of predictive values for height and
nasal resistance in the decongested nose that are
useful in assessing the extent of any deviation from
normality in patients with nasal skeletal stenosis.
Total nasal resistance gives an overall measure of
nasal function but is a very crude measure as it
provides no information about the separate nasal
passages. Rhinologists have a dilemma when assessing nasal function as the nose consists of two separate dynamic airways. The ophthalmologist or
audiologist would never consider using a bilateral

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R. Eccles

measure of vision or hearing when assessing function

as this measure could fail to detect blindness in one
eye or deafness in one ear. Similarly, the measurement of total resistance may fail to detect unilateral
nasal obstruction. However, it is not very informative
to quote the mean of unilateral resistance when measured over a period of several hours because this
mean value will have a large standard deviation due
to the instability of unilateral resistance. The range of
unilateral nasal airway resistance in a group of
healthy volunteers when recorded over a 6 8-h period has been shown to vary from 0.36 to 1.36 Pa cm3
s (49) and from 0.28 to 0.63 Pa cm3 s (50). This
indicates that there is often almost a fourfold change
in unilateral resistance associated with the spontaneous congestion and decongestion of the nasal
venous sinuses.
One way to overcome the dilemma of spontaneous
changes in unilateral nasal resistance is to decongest
the nose prior to assessment. This solution was discussed above and is of use to the surgeon who is only
interested in assessing the extent of any nasal
anatomical problem (48). However, decongestion of
the nose is of no use in studying nasal physiology as
it is the spontaneous changes in unilateral resistance
that are of interest to the physiologist. One solution is
to quantify the extremes of unilateral resistance or
the amplitude of the unilateral changes in resistance
which occur over a period of several hours. This
approach has been used to determine the unilateral
changes in resistance in healthy subjects (51) and in
patients with common colds (49) and hay fever (52)
and to assess the effects of oral decongestants (53)
and the efficacy of nasal surgery (54). The disadvantage of unilateral nasal measurements is that, in order
to assess the amplitude of changes in unilateral nasal
resistance, it is necessary to make hourly measurements over a period of several hours. The advantage
of unilateral measurements is that they give a comprehensive assessment of the dynamic nose rather
than the crude snapshot that is provided by a single
measure of total resistance.
Nasal cycle
There are many descriptions in the literature of the
spontaneous and often reciprocal changes in human
nasal airflow which are usually termed the nasal cycle
(5557). In this review the term nasal cycle will be
used to mean spontaneous and often reciprocal
changes in unilateral nasal airflow associated with
congestion and decongestion of the nasal venous
sinuses.
Spontaneous changes in unilateral congestion and
decongestion of nasal venous sinuses were first described in the scientific literature by Kayser (1) but

Acta Otolaryngol 120

they were known to the ancient Hindus as early as

the Vedic period (58). Some of the earliest studies
involved direct visual observations of the reactions
of the nasal mucosa and described reciprocal changes
of congestion and decongestion of the nasal turbinates. Heetderks (59) stated that The turbinates of
one side of the nose were filling whilst the other side
was throwing off secretion. When the filling of the
turbinates on one side had reached its maximum, the
turbinates on the other side were completely empty,
thus affording much breathing space.
Heetderks (59), in his study of 60 healthy volunteers, found that in 80% of cases there was a definite
cycle of reaction and this statement has been used
many times in the literature to support the idea that
80% of the population exhibit a so-called nasal cycle.
However, closer examination of the phenomenon led
Gilbert and Rosenwasser (60) to conclude that Despite its appearance in medical textbooks there is
little empirical support for the nasal cycle as strictly
defined, that is, as a reciprocal and rhythmically
alternating relation between the two nasal passages,
with identical periods, mean levels, and amplitude in
each.
One problem in determining the incidence of the
nasal cycle in a healthy population is that there is no
agreement of a definition as to which changes in nasal
airflow actually constitute a nasal cycle. Heetderks
(59), Stoksted (55) and Hasegawa and Kern (56) were
satisfied with the presence of reciprocal changes in
congestion and airflow as a criterion for the presence
of a nasal cycle and they found that between 7080%
of their study population fulfilled this criterion.
Gilbert (60) used autocorrelation as a measure of
rhythmicity and found that bilateral rhythmicity was
present in only 2 out of 16 healthy volunteers (13%);
however, bilateral reciprocity was found in 7 out of
16 volunteers, indicating that reciprocal changes in
nasal airflow were found in almost half the
population.
In a study by Flanagan and Eccles (50) on 52
healthy volunteers unilateral nasal airflow was measured every hour over an 8-h period and a wide range
of patterns of airflow was observed, with some volunteers exhibiting regular spontaneous and reciprocal
changes in unilateral airflow whilst others exhibited
irregular changes in airflow. The authors defined a
nasal cycle in terms of a numerical classification that
encompassed the correlation between unilateral nasal
airflow changes and the distribution of airflow between the nasal airways in each subject and concluded that only 21% (11 of the 52 volunteers)
exhibited airflow patterns that could be defined as a
nasal cycle in these terms. When present, the reciprocal changes in nasal airflow have been reported to
occur on a timescale of 0.53.0 h (5557).

Acta Otolaryngol 120

The spontaneous, and often reciprocal, changes in

nasal airflow are caused by congestion and decongestion of nasal venous sinuses under the influence of the
sympathetic nervous system (17). Section or local
anaesthesia of the cervical sympathetic nerve which
supplies one side of the nose and face causes ipsilateral nasal congestion and abolition of the spontaneous changes in nasal airflow (30, 31).
Our understanding of the factors that may influence the spontaneous and reciprocal changes in nasal
airflow is very limited. The idea that the nasal cycle
may act to share the burden of air conditioning
between the two nasal passages so that dominance of
airflow alternates over the course of several hours is
an attractive hypothesis. If nasal airflow in some way
influenced the control of the nasal cycle then one
would expect that the spontaneous changes in the
nasal venous sinuses would not occur in the absence
of nasal airflow. However, there is some evidence that
spontaneous congestion and decongestion of nasal
blood vessels still occur in the laryngectomized patient in the absence of any nasal airflow (61, 62).
Some reports in the literature of Yoga state that
dominance of nasal airflow may be changed by
breathing exercises (pranayama) (63) but studies
on different breathing patterns have failed to substantiate any such effect of nasal breathing (64). Thus
the present state of our knowledge does not provide
any support for the hypothesis that nasal airflow in
some way influences the nasal cycle.
The spontaneous changes in nasal airflow associated with the nasal cycle may be related to oscillations in the activity of autonomic control centres in
the central nervous system and this will be discussed
below.
Central control of nasal airflow
The idea that the spontaneous changes in nasal
airflow associated with the nasal cycle may be controlled from some centre in the brain was first put
forward by Stoksted (55) in 1953 who speculated that
the nasal cycle was regulated by a central sympathetic centre possibly situated in the hypothalamus.
Studies on anaesthetized animals have demonstrated
that pronounced nasal vasoconstriction and a reduction in nasal airway resistance (15, 21) may be induced on electrical stimulation of areas of the
hypothalamus, indicating that this area of the brain
does have an influence on nasal vasomotor activity.
However, the nasal vasoconstrictor responses may be
related more to a generalized vasoconstrictor response rather than to specific control of the nasal
cycle. Hypothalamic stimulation caused bilateral
nasal vasoconstrictor responses but was not associated with any reciprocal changes in nasal vasomotor

Nasal airflow in health and disease

585

Fig. 2. Model to illustrate the sympathetic nervous control

of nasal venous sinuses. Vasomotor control is proposed to
reside in two half centres in the brainstem. The half centres
have reciprocal connections so that the dominance of activity oscillates over a period of hours, with only one centre
having dominance at any time. The sympathetic vasoconstrictor tone exerted by the right and left cervical sympathetic nerves which supply the two halves of the nose is
normally asymmetrical. The asymmetrical sympathetic tone
causes decongestion of the venous sinuses on one side of
the nose and congestion on the other side. The spontaneous
changes in nasal congestion occurring over a period of
hours are often called a nasal cycle.

activity and this indicates that the hypothalamus may

be associated with the control of a defence reaction
rather than the control of the nasal cycle (21).
Reciprocal nasal vasomotor responses with ipsilateral vasoconstriction and contralateral vasodilation
have been initiated on electrical stimulation of areas
of the brain stem in the anaesthetized cat (65). The
reciprocal nasal vasomotor responses were proposed
to originate from groups of neurones on either side of
the brainstem that acted as oscillators and controlled
the sympathetic tone to each side of the nose. By
stimulation of first one side of the brainstem and then
the other, the dominance of sympathetic tone to nasal
blood vessels could be switched from one side to the
other, with a reciprocal relationship between the two
halves of the brainstem (65). These switches in nasal
sympathetic vasomotor activity could also occur
spontaneously and were closely linked to the control
of respiration (66).
At present our understanding of the central control
of nasal airflow is limited to animal experiments but
this knowledge has allowed the development of a
model of a control system (22) as illustrated in Fig. 2.

586

R. Eccles

Effect of changes in posture on nasal airflow

The changes in nasal airflow associated with changes
in posture may be explained by two separate mechanisms: an increase in central venous pressure on
moving from erect to supine; and a reflex change in
nasal vasomotor activity on adoption of the lateral
recumbent position. The postural changes in nasal
airflow can be demonstrated in healthy volunteers;
they are often exaggerated in patients with rhinitis
and may cause complete unilateral or total nasal
obstruction (6769).
The effects of an increase in venous pressure on
nasal airflow were first noted by Sternberg in 1925
(11), who stated that an elevation of venous pressure
in anaesthetized animals caused swelling of the nasal
mucosa. In 1938 van Dishoeck reported the first
human study and found that compression of the
jugular vein caused ipsilateral swelling of the nasal
mucosa (70). The changes in pressure in the human
internal jugular vein associated with changes in posture were studied by Jonson and Rundcrantz in 1969
(71), who reported that the change from sitting to
recumbent posture caused an increase in venous pressure of up to 8 mmHg. Rundcrantz (72) also studied
the effects of postural changes on nasal airflow in
patients with rhinitis and demonstrated that when
these patients were placed in a head-down posture
there was a large increase in total nasal resistance to
airflow.
The increase in venous pressure associated with a
change from sitting to supine causes an increased
filling of the nasal venous sinuses and an increase in
nasal resistance to airflow. This passive hydrostatic
effect of increased venous pressure is superimposed
on any asymmetry of the nasal venous sinuses associated with the nasal cycle. The side of the nose with
the greatest level of congestion in general exhibits the
greatest increase in congestion and may become completely obstructed (73). The unilateral nasal obstruction may be caused to alternate from one side of the
nose to the other by adoption of the lateral recumbent position, so that the downside nasal passage
congests and the upside decongests. This is not a
passive effect of any further change in venous pressure but is a reflex change in vasomotor activity
associated with a pressure stimulus to one side of the
body.
The pressure response to the axilla region associated with adoption of the lateral recumbent position
can be mimicked by application of a crutch to the
axilla region whilst sitting, and this procedure has
been shown to cause ipsilateral nasal congestion and
contralateral decongestion (63, 74, 75). The procedure of using a wooden crutch (Yoga Danda) to

Acta Otolaryngol 120

initiate changes in nasal airflow has been known to

the practitioners of Yoga for many hundreds of years
and is frequently described in the literature of Yoga
(63). The reciprocal changes in nasal airflow observed
on adoption of the lateral recumbent position are
caused by pressure upon the axilla and hip regions as
these body surfaces have been shown to be the most
sensitive regions to elicit the nasal response (76).
Local anaesthesia to the skin surface of the axilla
does not abolish the response but intercostal nerve
block does abolish the nasal response to axillary
pressure (76).
The reciprocal changes in nasal airflow associated
with the lateral recumbent position may have a functional significance as the reflex ensures that the upper
nasal passage has the dominant airflow. In persons
with a marked asymmetry in nasal airflow associated
with the nasal cycle it would seem to be a functional
advantage to decongest the upper nasal passage on
adoption of the lateral recumbent position as the
dependent nasal passage could be obstructed by physical contact with the ground.
Pressure to the axilla not only influences nasal
airflow but also causes changes in sweating, with
ipsilateral inhibition and contralateral facilitation (77,
78). This response would also seem to have some
functional basis as sweating on the downside in contact with the ground would not aid cooling whereas
sweating on the exposed upper surface would be
effective. Both the sweating and nasal responses are
mediated by sympathetic nerves and presumably the
afferent pathway from the body surface pressure
receptors must trigger a reciprocal change in sympathetic tone to the nose and skin.
Effect of exercise on nasal airflow
Exercise causes a generalized increase in sympathetic
nervous activity, with increases in heart rate and
bronchodilation and a decrease in nasal resistance to
airflow. The first study on the effects of exercise on
nasal resistance was conducted by Richardson and
Seebohm in 1968 (79) and they demonstrated that
when patients with allergic rhinitis performed strenuous exercise there was a marked reduction in nasal
airway resistance. These authors also established that
the reduction in nasal airway resistance was due to an
increase in sympathetic vasoconstrictor tone to the
nasal venous sinuses as the response was reduced by
topical application of phentolamine or local anaesthesia of the stellate ganglion.
The nasal response to exercise has been studied
subsequently in healthy volunteers (80, 81) and in
patients with asthma and rhinitis (82, 83) and has
also been used as a means of decongesting the nose in
the assessment of patients prior to nasal surgery (48).

Acta Otolaryngol 120

It has some functional significance as it reduces the

work of breathing by lowering nasal resistance to
airflow. However, exercise is normally accompanied
by a switch to mouth breathing at a work rate of
around 105 W (84) and therefore the nasal response
is probably only of significance for low-to-moderate
work rates when a significant proportion of the tidal
volume passes through the nose.
Effect of hyper6entilation and rebreathing on nasal
airflow
The partial pressure of carbon dioxide in arterial
blood is the major factor which influences ventilation
via peripheral and central chemoreceptors. The partial pressure of carbon dioxide in the arterial blood
can be lowered by hyperventilation and increased by
breath holding or asphyxia. These changes in the
partial pressure of carbon dioxide are accompanied
by changes in the drive to breathe and by changes in
nasal airway resistance.
Tatum in 1923 (85) studied the effects of partial
asphyxia and hyperventilation on nasal volume in
anaesthetized dogs and rabbits and demonstrated
that asphyxia caused a nasal vasoconstrictor response
whereas hyperventilation caused nasal vasodilation.
The nasal vasoconstrictor response to partial asphyxia was abolished on section of the cervical sympathetic nerves whereas the vasodilator response to
hyperventilation was unaffected. Tatum also reported
that in humans rebreathing from a bag or a prolonged breath hold caused a decrease in nasal airway
resistance whereas hyperventilation caused an increase in nasal airway resistance.
The experimental work of Tatum has been repeated in both animals and humans (80, 86 89) and
the results of these studies confirm his conclusions
that changes in blood carbon dioxide levels influence
nasal airway resistance via the sympathetic nerve
supply to nasal blood vessels.
The nasal vasoconstrictor response to an elevation
in blood carbon dioxide can be explained by a reflex
increase in sympathetic nervous activity mediated by
peripheral and central chemoreceptors. The reduction
in nasal airway resistance associated with asphyxia
and rebreathing has some functional significance as
the increase in nasal patency will facilitate ventilation. The nasal vasodilator response to a decrease in
blood carbon dioxide is more difficult to explain as it
is unaffected by section of the sympathetic nerves (85)
and may be mediated by parasympathetic pathways
(88).
Endocrine influence on nasal airflow
The development and activity of the nasal mucosa is
influenced by many hormones but of these it is

Nasal airflow in health and disease

587

adrenaline secreted from the adrenal medulla which

has the most obvious and acute effect (17).
Adrenaline is released in response to stressful stimuli
such as pain and asphyxia and causes a pronounced
nasal vasoconstriction and a reduction in nasal airway resistance. The nasal blood vessels are extremely
sensitive to circulating adrenaline, being up to four
times as sensitive as those of the heart (15).
There is much clinical and experimental evidence
which indicates that the male and female sex hormones have an influence on the nose. Nasal obstruction and hypersecretion are often associated with
puberty, menstruation and pregnancy (9093).
Nasal airflow in animals
Much of the experimental work on the nose has been
done on animals such as the cat, dog, pig, rabbit, rat
and ferret. Of these animals the domestic pig has the
nasal structure that most closely resembles that of
humans, with a much simpler nasal turbinate structure than other experimental animals (31). The nasal
turbinate structure in most animals other than humans and primates is exceedingly complex, with numerous layers of delicate scroll-like turbinates in most
animals (94). Much work has been reported on the
autonomic innervation of the nose in animals using
the technique of nasal plethysmography as reviewed
above. Relatively few investigators have recorded
nasal airflow directly and most have resorted to
indirect methods of determining nasal resistance, such
as determining pressure changes associated with a
passive airflow through the nose (31, 95). Nasal
airflow in many animals is involved in thermoregulation as the nose acts as a heat exchanger and may be
involved in the regulation of brain temperature (96).
In those animals that have been studied the nasal
airflow and degree of nasal congestion are often
found to be asymmetrical and to exhibit spontaneous
and often reciprocal responses (31, 9799).
Cerebral effects of nasal airflow
The literature of Yoga describes breathing exercises
which often involve unilateral nasal airflow and
which are believed to alter mood and cerebral activity
(100). There is much supporting evidence from the
scientific and clinical literature that airflow through
the nose can influence cerebral activity. Deep nasal
breathing has been shown to have an activating effect
on the electroencephelogram (EEG) in humans to
such an extent that it can trigger epileptic abnormalities in susceptible persons (101, 102). This arousal
effect of nasal airflow was not caused by any change
in blood gases due to hyperventilation as passive
airflow through the nose had similar effects to hyperventilation and the activating effect of nasal airflow

588

R. Eccles

was suppressed by local anaesthesia of the nasal

mucosa. Other human experiments have demonstrated that the effects of nasal airflow are lateralized
with EEG activation occurring with the dominant
airflow (103). An alternation of cerebral activity has
been reported to occur with the alternations in nasal
airflow associated with the nasal cycle, with cerebral
activation contralateral to the dominant nasal airflow
(104).
Any effects of nasal airflow on cerebral activity are
likely to be mediated via nasal trigeminal nerves,
although some influence of the olfactory nerves cannot be excluded.
Sensation of nasal airflow
The cool sensation of nasal airflow we feel with each
inspiration is mediated by cold receptors in the nose
which are supplied by branches of the trigeminal
nerves (105, 106). The sensation of nasal airflow is
mainly related to a cool sensation in the nose rather
than to sensations from the respiratory muscles or
lungs, and blockade of the trigeminal nerves supplying the nose or local anaesthesia of the nasal epithelium cause a sensation of nasal obstruction (107,
108).
The sensation of nasal airflow is increased by topical nasal application or inhalation of menthol and
this provides a false sensation of decongestion and
improved airflow (109). Oral administration of menthol by means of a lozenge causes a similar sensation
of nasal coolness and increased nasal airflow (110).
The effects of ingestion of a menthol lozenge on the
subjective sensations of nasal airflow and total nasal
airway resistance are illustrated in Fig. 3. Menthol is
believed to influence the activity of cold receptors by
altering the conductance of calcium ions across the
nerve cell membrane (111 113). Menthol may have a
specific pharmacological effect on cold receptors, as
L-menthol has cooling properties whereas D-menthol
has little cooling activity (114), and by manipulating
the chemical structure of menthol analogues it is
possible to produce cooling compounds that are more
potent than menthol (113, 115).
Menthol is widely used as an ingredient of common cold medications, candy, chewing gum,
cigarettes and snuff; the popularity of menthol-containing products may be related to the pleasant and
satisfying effect of menthol on the drive to breathe
(116).
PATHOPHYSIOLOGY OF NASAL AIRFLOW
The inflammatory responses accompanying rhinitis
involve a complex mixture of mediators. However,
with allergic rhinitis the dominant inflammatory me-

Acta Otolaryngol 120

diator is histamine and with infectious rhinitis

bradykinin dominates the inflammatory soup of mediators (117). With few exceptions inflammatory mediators such as prostaglandins, tachykinins, etc. cause
vasodilation and nasal congestion. Only the pathophysiology relevant to the control of nasal airflow
will be presented as a discussion of rhinitis and
inflammation is beyond the remit of the present review and has been reviewed extensively elsewhere
(118, 119).
Rhinitis is an inflammatory response of the nasal
epithelium which is commonly caused by nasal infection or allergy and which may also be associated with
nasal irritation due to chemical or mechanical assaults on the nose, such as those associated with air
pollution.
The nasal inflammatory response causes the generation of a complex mixture of vasodilator mediators.
The vasodilator response is likely to be the same in
each nasal airway but it will be superimposed on any
asymmetry of sympathetic vasoconstrictor tone associated with the nasal cycle. The vasodilator effect of
the inflammatory mediators is likely to be limited on
the side of the nose with a high sympathetic tone and
will therefore have little effect on nasal airflow. How-

Fig. 3. The effects of ingestion of a menthol or placebo

lozenge on subjective sensation of nasal congestion and
nasal resistance to airflow in human volunteers with a
common cold: (
, ) mean values for the menthol-treated
group; ( , ) values for the placebo-treated group. The
subjective sensation of nasal congestion was significantly
reduced 10 min after ingestion of the menthol lozenge but
nasal airway resistance as measured by rhinomanometry
was unaffected. The congestion score represents change in
score on a 100 mm visual analogue scale. Nasal resistance
is in Pa cm3 s. Results taken from Eccles et al. (110).

Acta Otolaryngol 120

Nasal airflow in health and disease

589

whereas another study has reported no change in

total nasal airflow in the pollen season despite patients reporting a sensation of nasal obstruction during this time (52).
PHARMACOLOGY OF NASAL AIRFLOW
Almost any substance which has an effect on vascular
smooth muscle will have some influence on nasal
airflow by causing changes in the activity of the
smooth muscle of nasal venous sinuses. Similarly, any
substance which influences the activity of sympathetic
noradrenergic nerve endings is likely to influence
nasal airflow by altering the sympathetic vasoconstrictor tone to nasal venous sinuses. Only the pharmacology relevant to effects on nasal airflow will be
discussed.

Fig. 4. Spontaneous changes in unilateral nasal airway

resistance recorded in one subject while suffering from
symptoms of common cold and 68 weeks later when
healthy: () left nasal airway resistance; ( ) right nasal
airway resistance. Redrawn from Eccles et al. (49).

ever, on the side of the nose with a low sympathetic

tone the vasodilator response may be unopposed,
causing a large decrease in airflow and occasionally
complete unilateral nasal obstruction.
The overall effect of the vasodilation associated
with rhinitis is to cause an increase in the amplitude
of the spontaneous changes in nasal airflow associated with the nasal cycle. Such an increase in amplitude in the nasal cycle has been reported for rhinitis
associated with common cold (49, 120) and the
changes in airflow in healthy subjects and those with
the common cold are illustrated in Fig. 4.
One would expect the changes in nasal airflow
associated with allergic rhinitis to be similar to those
associated with infectious rhinitis as both diseases
involve inflammation of the nasal epithelium and the
generation of vasodilator mediators. However, there
is little information on the changes in nasal airflow
associated with allergic rhinitis; one study on patients
with seasonal allergic rhinitis has reported a decrease
in total nasal airflow during the pollen season (121),

Sympathomimetics and sympatholytics

The nasal blood vessels are extremely sensitive to
sympathomimetic medications as they mimic the
vasoconstrictor effects of noradrenaline/adrenaline
and cause decongestion of nasal venous sinuses and a
decrease in nasal resistance to airflow. Nasal decongestant medications are sympathomimetics which act
on alpha 1 and alpha 2 receptors on nasal venous
sinuses. There is some evidence that alpha 1 receptors
may be the major receptor type on the smooth muscle
of nasal venous sinuses (122). The pharmacology of
sympathomimetics and nasal decongestants has recently been reviewed (123). Repeated application of
topical sympathomimetics can cause a rebound vasodilation and nasal congestion (124, 125) which may
be related to tissue hypoxia cause by pronounced
vasoconstriction. Rhinitis medicamentosa can occur
after prolonged abuse of topical nasal decongestants
(126, 127) and this condition may be more related to
chronic exposure to the preservatives used in topical
nasal decongestants than to vasoconstriction (125).
Sympatholytic medications may cause nasal congestion by means of their inhibitory effects on the
sympathetic nervous system and this is a very common side-effect associated with medications such as
reserpine (126).
Although one might expect that the decongestion
caused by treatment with a topical nasal decongestant
sympathomimetic medication would be greater than
that associated with spontaneous decongestion associated with the nasal cycle, the magnitude of the
pharmacological and physiological decongestion
effects has in fact been shown to be equivalent (128).
Histamine and antihistamines
Histamine is a potent vasodilator mediator associated
with the inflammatory allergic response. Histamine

590

R. Eccles

has effects on nasal sensory nerves and blood vessels

and causes sneezing, itching, runny nose and nasal
congestion (129). It is the vasodilator action of histamine that influences nasal airflow by causing congestion of the nasal venous sinuses. Histamine
challenge is often used as an experimental method to
elicit nasal congestion and other symptoms of nasal
allergy (36, 130, 131).
The effects of histamine on the human nose are
mediated by both H1 and H2 receptors and both
these receptors are involved in the dilation of venous
sinuses, whereas only the H1 receptors are involved
in sneezing, itching and hypersecretion (132). The
involvement of both H1 and H2 receptors in nasal
congestion may explain why antihistamines which are
H1 receptor antagonists are relatively ineffective in
treating nasal congestion associated with nasal allergy
and histamine challenge (132, 133).
Bradykinin
The kallikrein enzyme responsible for the generation
of bradykinin was first shown to be present in the
nose, in cat nasal secretions (134). Bradykinin is a
potent vasodilator mediator associated with the inflammatory response to acute upper respiratory tract
infection (135). Bradykinin has effects on both nasal
blood vessels and nasal sensory nerves, causing nasal
congestion, nasal irritation and runny nose (136,
137). Although there has been considerable research
undertaken to discover a bradykinin antagonist that
could be useful in the treatment of symptoms associated with acute upper respiratory tract infection,
rather as antihistamines are utilized in the treatment
of allergic rhinitis, at present no bradykinin antagonist is available for the treatment of nasal disease
(138).
Corticosteroids
Intranasal corticosteroids are widely used for the
treatment of allergic rhinitis but there are very few
studies on the effects of corticosteroids on nasal
airflow. Unlike the antihistamines, which have no
effect on nasal congestion, intranasal corticosteroids
are generally believed to provide relief for the symptom of nasal congestion associated with allergic rhinitis (139). Topical nasal steroid treatment has been
shown to reduce the increase in nasal airway resistance associated with nasal challenge with grass pollen in allergic patients (140). Following dermal
application, corticosteroids induce a pallor of the
skin, which has been used to grade their anti-inflammatory potency, but there is no evidence to indicate
that corticosteroids cause vasoconstriction of nasal
blood vessels (139).

Acta Otolaryngol 120

EFFECTS OF SURGERY ON NASAL

AIRFLOW
As discussed in the introduction to this review, nasal
surgery is primarily performed to restore the respiratory function of the nose by improving nasal airflow.
The dilemma faced by the surgeon is that the subjective symptom of nasal obstruction as reported by the
patient does not always relate to an objective limitation of nasal airflow. A poor correlation between
subjective and objective measures of nasal airflow has
been previously reported (141143) and this means
that it is important to properly assess the extent of
any nasal obstruction before treatment with nasal
surgery. The most relevant assessment in this case
would be the measurement of nasal airflow but this
assessment is not available in most clinics and the
surgeon must rely on other subjective assessments of
obstruction, such as visual inspection of the nose via
rhinoscopy.
Even in those clinics where rhinomanometry is
available to measure nasal airflow prior to surgery
there are still several problems. A major problem is
that there is no generally accepted standard minimum
level of nasal airflow that is compatible with normal
nasal function. Broms (48) has described normal
values of nasal airflow following decongestion (induced by standardized physical exercise) and related
nasal airflow to height so that it is possible to predict
what a healthy patients normal airflow should be by
measuring their height. This work is of great clinical
significance as it provides the upper and lower limits
of normal total and unilateral nasal airflow, which
are of great value to the surgeon in deciding if nasal
surgery can provide any benefit (48). However, these
data may only be applicable to the Scandinavian
population.
Normal values for nasal airflow in a Finnish population have been used to great advantage in assessing
patients waiting for septoplasty, as only those patients whose total nasal airflow was below normal
were operated on, and this protocol allowed a great
reduction in the waiting list of patients (144).
The causes of nasal obstruction can be classified
into two types by the use of a topical nasal decongestant: anatomical obstruction due to a hard tissue
problem, such as a deviated nasal septum; and physiological obstruction due to nasal inflammation and
swelling of the nasal epithelium (145). McCaffrey
(145) provides some normal values for total and
unilateral nasal resistance pre- and post-decongestion
and states that a marked reduction in nasal resistance
after decongestion to a normal value suggests that
mucosal disease (e.g. allergic rhinitis, rhinitis medicamentosa) is a major contributor to the nasal obstruc-

Acta Otolaryngol 120

Nasal airflow in health and disease

591

structed state of the nasal passage and this may be

a more relevant parameter than total nasal airflow
in assessing the severity of nasal obstruction. The
effects of surgery on the spontaneous changes in
nasal airflow in one patient are illustrated in Fig.
5, and it is apparent from this Figure that submucosal diathermy causes a reduction in the amplitude
of the nasal cycle which may be explained by cauterization of the venous sinuses in the nasal epithelium.
Fig. 5. Spontaneous changes in total and unilateral nasal
airflow (measured by posterior rhinomanometry at a fixed
sample pressure of 75 Pa) in one patient with chronic
rhinitis before and 23 months after surgical treatment
with submucosal diathermy to the inferior turbinate. Redrawn from Quine et al. (54).

tion. In contrast, if decongestion results in B 35%

decrease in resistance, and especially if asymmetry
of airflow persists, a structural problem (septal deformity, conchal hypertrophy, stenosis or concha
bullosa) can be inferred. Nasal airflow limitation
due to alar collapse can be diagnosed by observing
the alar wings of the nose during a deep inspiration
or by measuring changes in airflow at high inspiratory pressures (145).
A problem with the assessment of nasal airflow
as a criterion for nasal surgery is that nasal airflow
is often unstable due to the spontaneous changes in
airflow associated with the nasal cycle. A single
measurement of total nasal airflow can only provide
very limited information about nasal function as
airflow may fluctuate widely throughout the day. A
comprehensive assessment of nasal airflow would
involve serial measurements of unilateral airflow
over a period of several hours and, although this is
impractical as a routine clinical assessment, this
type of study can provide valuable information
about the pathophysiology of nasal airflow and the
effects of nasal surgery.
In a study on the effects of submucosal
diathermy on nasal airflow in patients with chronic
rhinitis serial measurements of nasal airflow were
made over a period of 5 h, both before and 23
months after nasal surgery (54). Unilateral nasal
airflow was measured as the minimum (Fmin) and
maximum (Fmax) airflow in each nasal passage
over the 5-h recording period. Unilateral measures
of airflow proved to be much more sensitive than
total nasal airflow as a measure of the effects of
the surgery. Fmin increased by 133% following
surgery whereas total nasal airflow only increased
by 51%. Fmin provides a measure of the most ob-

CONCLUSIONS
At present the measurement of nasal airflow is only
performed in specialized research centres and does
not have a routine clinical application. However, if
progress is to be made in the diagnosis and treatment of nasal disease then measurement of the respiratory function of the nose is just as important to
the rhinologist as respiratory function measurements are to the pneumologist.

REFERENCES
1. Kayser R. Die exacte messung der luftdurchgangigkeit
der nase. Arch Laryngol Rhinol 1895; 3: 101 20.
2. Wright JW. A consideration of the vascular mechanism of the nasal mucous membrane and its relations
to certain pathological processes. Am J Med Sci 1895;
109: 516 23.
3. Burnham HH. A clinical study of the inferior turbinate cavernous tissue; its divisions and their significance. Can Med Assoc J 1941; 44: 477 81.
4. Cauna N. Blood and nerve supply of the nasal lining.
In: Proctor DF, Andersen I, eds. The nose, upper
airways physiology and the atmospheric environment.
Amsterdam: Elsevier, 1982: 45 69.
5. Haight JSJ, Cole P. Site and function of the nasal
valve. Laryngoscope 1983; 93: 49 55.
6. van Dishoek HAE, Leiden MD. The part of the valve
and the turbinates in total nasal resistance. Int Rhinol
1965; 3: 19 26.
7. Bridger GP. Physiology of the nasal valve. Arch Otolaryngol 1970; 92: 543 53.
8. Cole P. The respiratory role of the upper airways. A
selective clinical and pathological review. St Louis,
MO: Mosby Year Book, 1993: 164.
9. Jones AS, Lancer JM. Does submucosal diathermy to
the inferior turbinate reduce nasal resistance to
airflow in the long term? J Laryngol Otol 1987; 101:
448 51.
10. Tschalussow MA. Innervation der gefasse der nasenschleimhaut. Pflugers Arch 1913; 151: 523 42.
11. Sternberg H. Beitrage zur Physiologie und Pathologie
der Schleimhaut der Luftwege. Z Hals-Nasen-u
Ohrenheilk 1925; 12: 340 64.
12. Undritz W. Uber Vasomotorische Reflexe der Nase. Z
Hals-Nasen-u Ohrenheilk 1929; 25: 157 86.
13. Blier Z. Physiology of the Sphenopalatine Ganglion.
Am J Physiol 1930; 93: 398 406.

592

R. Eccles

14. Slome D. Physiology of nasal circulation. Lect Sci

Basis Med 1955; 5: 45168.
15. Malcolmson KG. The vasomotor activities of the
nasal mucous membrane. J Laryngol Otol 1959; 37:
7398.
16. Eccles R, Wilson H. The autonomic innervation of
the nasal blood vessels of the cat. J Physiol 1974; 238:
54960.
17. Eccles R. Neurological and pharmacological considerations. In: Proctor DF, Andersen I, eds. The nose,
upper airways physiology and the atmospheric environment. Amsterdam: Elsevier, 1982: 191214.
18. Eccles R, Wilson H. The parasympathetic secretory
nerves of the nose of the cat. J Physiol 1973; 230:
21323.
19. Agarwal PN. Bilateral vidian neurectomyIndications and results. J Laryngol Otol 1977; 91: 235 40.
20. Uddman R, Alumets J, Densert O, Hakanson R,
Sundler F. Occurrence and distribution of vip nerves
in the nasal mucosa and tracheobronchial wall. Acta
Otolaryngol (Stockh) 1978; 86: 4438.
21. Eccles R, Lee RL. The influence of the hypothalamus
on the sympathetic innervation of the nasal vasculature of the cat. Acta Otolaryngol (Stockh) 1981; 91:
12734.
22. Eccles R. Sympathetic control of nasal erectile tissue.
Eur J Respir Dis 1983; 64: 1504.
23. Dahlstrom A, Fuxe K. The adrenergic innervation of
the nasal mucosa of certain mammals. Acta Otolaryngol (Stockh) 1964; 59: 6572.
24. Anggard A, Edwall L. The effects of sympathetic
nerve stimulation on the tracer disappearance rate and
local blood content in the nasal mucosa of the cat.
Acta Otolaryngol (Stockh) 1974; 77: 1319.
25. Malm L. Sympathetic influence on the nasal mucosa.
Acta Otolaryngol (Stockh) 1977; 83: 201.
26. Lacroix JS, Stjarne P, Anggard A, Lundberg JM.
Sympathetic vascular control of the pig nasal mucosa
(III): co-release of noradrenaline and neuropeptide Y.
Acta Physiol Scand 1989; 135: 1728.
27. Cauna N, Cauna D. The fine structure and innervation of the cushion veins of the human nasal respiratory mucosa. Anat Rec 1975; 181: 116.
28. Burnham HH. An anatomical investigation of blood
vessels of the lateral nasal wall and their relation to
turbinates and sinuses. J Laryngol Otol 1935; 50:
56993.
29. Beickert P. Halbseitenrhythmus der vegetativen innervation. Arch Ohren-Nasen Kehlkopifheikonde 1951;
157: 40411.
30. Stoksted P, Thomsen K. Changes in the nasal cycle
under stellate ganglion blockade. Acta Otolaryngol
(Stockh) 1953; 109Suppl: 17681.
31. Eccles R. The domestic pig as an experimental animal
for studies on the nasal cycle. Acta Otolaryngol
(Stockh) 1978; 85: 4316.
32. Eccles K, Eccles R. Nasal vasodilation induced by
electrical stimulation of the vagus nerve. Rhinology
1982; 20: 8992.
33. Wheatley JR, Amis TC, Engel LA. Nasal and oral
airway pressure-flow relationships. J Appl Physiol
1991; 71: 231724.
34. Schumacher MJ. Rhinomanometry. J Allergy Clin
Immunol 1989; 83: 7118.

Acta Otolaryngol 120

35. Cole P, Roithmann R, Roth Y, Chapnik JS. Measurement of nasal patency. A manual for users of the
Toronto systems and others interested in nasal patency measurement. Ann Otol Rhinol Laryngol 1997;
106 Suppl 171: 1 23.
36. Eccles R. Evaluation of the nasal airway and nasal
challenge. In: Mackay IS, Bull TR, eds. Scott-Browns
Otolaryngology. . Oxford: Butterworth-Heinemann,
1997: 4/4/14/4/15.
37. Grymer LF, Hilberg O, Elbrond O, Pedersen OF.
Acoustic rhinometry: evaluation of the nasal cavity
with septal deviations, before and after septoplasty.
Laryngoscope 1989; 99: 1180 7.
38. Roithmann R, Cole P, Chapnik J, et al. Acoustic
rhinometry in the evaluation of nasal obstruction.
Laryngoscope 1995; 105: 275 81.
39. Tomkinson A, Eccles R. Acoustic rhinometry. Curr
Opin Otolaryngol Head Neck Surg 1996; 4: 7 11.
40. Morris S, Jawad M, Eccles R. Relationships between
vital capacity, height and nasal airway resistance in
asymptomatic volunteers. Rhinology 1992; 30: 259
64.
41. Syaballo NC, Bundgaard A, Entholm P, Schmidt A,
Widicombe JG. Measurement and regulation of nasal
airflow resistance in man. Rhinology 1986; 24: 87
101.
42. Havas T, Gutierrez MC, Morton J, Rhodes L. Nasal
airway resistance in patients with cystic fibrosis. Aust
J Otolaryngol 1994; 1: 434 8:
43. Cole P. Nasal airflow resistance. In: Mathew OP,
SantAmbrogio, GNYMD, eds. Respiratory function
of the upper airway. New York: Marcel Dekker, 1988:
391 414.
44. Vig PS, Zajac DJ. Age and gender effects on nasal
respiratory function in normal subjects. Cleft Palate
Craniofac J 1993; 30: 279 84.
45. Polgar G, Kong GP. The nasal resistance of newborn
infants. J Pediatr 1965; 67: 557 67.
46. Stocks J, Godfrey S. Nasal resistance during infancy.
Respir Physiol 1978; 34: 233 46.
47. Jones AS, Viani L, Phillips D, Charters P. The objective assessment of nasal patency. Clin Otolaryngol
1991; 16: 206 11.
48. Broms P. Rhinomanometry. III. Procedures and criteria for distinction between skeletal stenosis and mucosal swelling. Acta Otolaryngol (Stockh) 1982; 94:
361 70.
49. Eccles R, Reilly M, Eccles KSJ. Changes in the amplitude of the nasal cycle associated with symptoms of
acute upper respiratory tract infection. Acta Otolaryngol (Stockh) 1996; 116: 77 81.
50. Flanagan P, Eccles R. Spontaneous changes of unilateral nasal airflow in man. A re-examination of the
nasal cycle. Acta Otolaryngol (Stockh) 1997; 117:
5905.
51. Flanagan P, Eccles R. The normal range of unilateral
nasal air-flow in healthy human volunteers. J Physiol
Lond 1996; 491P: P53 4.
52. Takeuchi H, Jawad MSM, Eccles R. Changes in
unilateral nasal airflow in patients with seasonal allergic rhinitis measured in and out of season. Auris
Nasus Larynx 2000; 27: 141 5.
53. Jawad SSM, Eccles R. Effect of pseudoephedrine on
nasal airflow in patients with nasal congestion associated with common cold. Rhinology 1998; 36: 736.

Nasal airflow in health and disease

Acta Otolaryngol 120

54. Quine SM, Aitken PM, Eccles R. Effect of submucosal diathermy to the inferior turbinates on unilateral and total nasal airflow in patients with rhinitis.
Acta Otolaryngol (Stockh) 1999; 119: 9115.
55. Stoksted P. Rhinometric measurements for determination of the nasal cycle. Acta Otolaryngol (Stockh)
1953; 109 (Suppl): 15975.
56. Hasegawa M, Kern EB. The human nasal cycle.
Mayo Clin Proc 1977; 52: 2834.
57. Eccles R. The central rhythm of the nasal cycle. Acta
Otolaryngol (Stockh) 1978; 86: 4648.
58. Sen H. Observations on the alternate erectility of the
nasal mucous membrane. Lancet 1901; 1: 564.
59. Heetderks DL. Observations on the reaction of normal nasal mucous membrane. Am J Med Sci 1927;
174: 23144.
60. Gilbert AN, Rosenwasser AM. Biological rhythmicity of nasal Aarway patencya re-examination of
the nasal cycle. Acta Otolaryngol (Stockh) 1987; 104:
1806.
61. Havas TE, Cole P, Gullane PJ, Kassel R, Kamino
D. The nasal cycle after laryngectomy. Acta Otolaryngol (Stockh) 1987; 103: 1116.
62. Fisher EW, Liu M, Lung VJ. The nasal cycle after
deprivation of airflow: A study of laryngectomy patients using acoustic rhinometry. Acta Otolaryngol
(Stockh) 1994; 114: 4436.
63. Bhole MV, Karambelkar PV. Significance of nostrils
in breathing. Yoga-Mimamsa 1968; 10: 112.
64. Mohan SM, Eccles R. Effect of inspiratory and expiratory airflow on congestion and decongestion in
the nasal cycle. Indian J Physiol Pharmacol 1989; 33:
1913.
65. Bamford OS, Eccles R. The central reciprocal control of nasal vasomotor oscillations. Pflugers Arch
Eur J Physiol 1982; 394: 13943.
66. Eccles R, Lee RL. Nasal vasomotor oscillations in
the cat associated with the respiratory rhythm. Acta
Otolaryngol (Stockh) 1981; 92: 35761.
67. Geterud A, Rundcrantz H. The effect of a local
decongestant in acute rhinitis as related to body position. Rhinology 1983; 21: 1558.
68. Hasegawa M, Saito Y. Postural variations in nasal
resistance and symptomatology in allergic rhinitis.
Acta Otolaryngol (Stockh) 1979; 88: 26872.
69. Hasegawa M. Posture induced nasal obstruction in
patients with allergic rhinitis. Clin Otolaryngol 1994;
19: 1357.
70. van Dishoeck HAE. Nasenplethysmometrials Mittel
zur Diagnose der Durchlassigkeit des Sinus sigmoideus und der Vena jugularis. Acta Otolaryngol
(Stockh) 1938; 26: 4552.
71. Jonson B, Rundcrantz H. Posture and pressure
within the internal jugular vein. Acta Otololaryngol
(Stockh) 1969; 68: 2715.
72. Rundcrantz H. Posture and congestion of nasal mucosa allergic rhinitis. Acta Otolaryngol (Stockh)
1969; 58: 2817.
73. Cole P, Haight JSJ. Posture and the nasal cycle. Ann
Otol Rhinol Laryngol 1986; 95: 2337.
74. Rao S, Potdar A. Nasal airflow with body in various
positions. J Appl Physiol 1970; 28: 1625.
75. Davies AM, Eccles R. Reciprocal changes in nasal
resistance to airflow caused by pressure applied to

76.
77.
78.
79.
80.

81.
82.

83.

84.
85.
86.

87.
88.

89.
90.
91.

92.
93.
94.
95.
96.

593

the axilla. Acta Otolaryngol (Stockh) 1985; 99: 154

9.
Haight JSJ, Cole P. Unilateral nasal resistance and
asymmetrical body pressure. J Otolaryngol 1986; 16
(15 Suppl): 1 31.
Takagi K, Kobayasi S. Skin pressure-vegetative
reflex. Acta Med Biol 1955; 4: 31 57.
Kuno Y. Human perspiration. 1956. Charles C.
Thomas, Springfield Illinois p. 204 11.
Richardson H, Seebohm P. Nasal airway response to
exercise. J Allergy 1968; 41: 269 84.
Dallimore NS, Eccles R. Changes in human nasal
resistance associated with exercise, hyperventilation
and rebreathing. Acta Otolaryngol (Stockh) 1977; 84:
416 21.
Forsyth RD, Cole P, Shephard RJ. Exercise and
nasal patency. J Appl Physiol 1983; 860 865.
Hasegawa M, Kabasawa Y, Ohki M, Watanabe I.
Exercise-induced change of nasal resistance in asthmatic children. Otolaryngol Head Neck Surg 1985;
93: 772 6.
Syaballo NC, Bundgaard A, Widdicombe JG. Effects
of exercise on nasal airflow resistance in healthy subjects and in patients with asthma and rhinitis. Bull
Eur Physiopathol Respir 1985; 21: 507 13.
Niinma V, Cole P, Mintz Z, Shepard RJ. The
switching point from nasal to oronasal breathing.
Respir Physiol 1980; 42: 61 71.
Tatum AL. The effect of deficient and excessive pulmonary ventilation on nasal volume. Am J Physiol
1923; 65: 229 33.
Hasegawa M, Saito Y, Watanabe K. Changes of
nasal airway resistance caused by breathing holding.
I. Results in normal subjects. Japanese Journal of
Otology (Tokyo) 1976; 89: 30 5.
McCaffrey TV, Kern EB. Response of nasal airway
resistance to hypercapnia and hypoxia in man. Ann
Otol Rhinol Laryngol 1979; 88: 247 52.
Babatola FDO, Eccles R. Nasal vasomotor responses
in man to breath holding and hyperventilation
recorded by means of intranasal balloons. Rhinology
1986; 24: 271 6.
McCaffrey TV, Kern EB. Response of nasal airway
resistance to hypercapnia and hypoxia in the dog.
Acta Otolaryngol (Stockh) 1979; 87: 545 53.
Chavanne L. Secretion nasale et glandes endocrines.
Ann Otolaryngol 1987; 5: 401 25.
Holmes H, Goodell H, Wolf S, Wolff HG. The nose.
An experimental study of reactions within the nose
in human subjects during varying life experiences.
Springfield, IL: Charles C. Thomas, 1950: 154.
Ellegard E, Karlsson G. Nasal congestion during the
menstrual cycle. Clin Otolaryngol Allied Sci 1994;
19: 400 3.
Ellegard E, Karlsson G. Nasal congestion during
pregnancy. Clin Otolaryngol 1999; 24: 307 11.
Negus V. The comparative anatomy and physiology
of the nose and paranasal sinuses. Edinburgh: E. &
S. Livingstone, 1958: 402.
Eccles R, Eccles KSJ. Sympathetic innervation of the
nasal mucosa of the pig. Res Vet Sci 1981; 30: 349
52.
Bamford OS, Eccles R. The role of sympathetic
efferent activity in the regulation of brain temperature. Pflugers Arch Eur J Physiol 1983; 396: 138
43.

594

R. Eccles

97. Bojsen-Moller F, Fahrenkrug J. Nasal swell bodies

and cyclic changes in the air passages of the rat and
rabbit nose. J Anat 1971; 110: 2537.
98. Webber RL, Jeffcoat MK, Harman JT, Ruttimann
UE. MR demonstration of the nasal cycle in the
beagle dog. J Comput Assist Tomogr 1987; 11: 869
71.
99. Reo NV, Barnett JKC, Neubecker TA, Alexander
ME, Goecke CM. A nuclear-magnetic-resonance investigation of the upper airways in ferrets. 1. Effects
of histamine and methacholine. Magn Reson Med
1992; 27: 2133.
100. Iyengar BKS. Light on Pranayama. Unwin Paperbacks: London, 1981: 296.
101. Kristof M, Servit Z, Manas K. Activating effect of
nasal air flow on epileptic electrographic abnormalities in the human EEG. Evidence for the reflex origin
of the phenomenon. Physiol Bohemoslovaca 1981; 30:
737.
102. Servit Z, Kristof M, Strejckova A. Activating effect of
nasal and oral hyperventilation on epileptic electrographic phenomena: Reflex mechanisms of nasal
origin. Epilepsia 1981; 22: 3219.
103. Werntz DA, Bickford RG, Shannahoff-Khalsa D.
Selective hemispheric stimulation by unilateral forced
nostril breathing. Human Neurobiol 1987; 6: 165 71.
104. Werntz DA, Bickford RG, Bloom FE, ShannahoffKhalsa DS. Alternating cerebral hemispheric activity
and the lateralization of autonomic nervous function.
Hum Neurobiol 1983; 2: 3943.
105. Eccles R. Effects of menthol on nasal sensation of
airflow. In: Green BG, ed. Chemical senses irritation. New York: Marcel Dekker, 1990: 275 95.
106. Clarke RW, Jones AS. Nasal airflow sensation [Editorial]. Clin Otolaryngol 1995; 20: 979.
107. Jones AS, Lancer JM, Shone G, Stevens JC. The
effect of lignocaine on nasal resistance and nasal
sensation of airflow. Acta Otolaryngol (Stockh) 1986;
101: 32830.
108. Jones AS, Crocher R, Wight RG, Lancer JM, Beckingham E. The effect of local anaesthesia of the nasal
vestibule on nasal sensation of airflow and nasal
resistance. Clin Otolaryngol 1987; 12: 4614.
109. Eccles R, Jones AS. The effect of menthol on nasal
resistance to air flow. J Laryngol Otol 1983; 97:
7059.
110. Eccles R, Jawad MS, Morris S. The effects of oral
administration of ( )-menthol on nasal resistance to
airflow and nasal sensation of airflow in subjects
suffering from nasal congestion associated with the
common cold. J Pharm Pharmacol 1990; 42: 652 4.
111. Isenberg C, Schafer K, Braun HA. The effect of
menthol on discharge pattern of cold receptors.
Pflugers Arch 1984; 400: R17.
112. Schafer K, Braun HA, Isenberg C. Effect of menthol
on cold receptor activity. J Gen Physiol 1986; 88:
75776.
113. Eccles R. Menthol and related cooling compounds. J
Pharm Pharmacol 1994; 46: 61830.
114. Eccles R, Griffiths DH, Newton CG, Tolley NS. The
effects of D and L isomers of menthol upon nasal
sensation of airflow. J Laryngol Otol 1988; 102: 506
8.
115. Watson HR, Hems R, Rowsell DG, Spring DJ. New
compounds with the menthol cooling effect. J Soc
Cosmetic Chemists 1978; 29: 185200.

Acta Otolaryngol 120

116. Eccles R. Role of cold receptors and menthol in thirst,

the drive to breathe and arousal. Appetite 2000; 34:
29 35.
117. Eccles R. Rhinitis as a mechanism of respiratory
defense. Eur Arch Otorhinolaryngol 1995; 252: S27.
118. Busse WW, Holgate ST, eds. Asthma and rhinitis.
Boston, MA: Blackwell Scientific Publications, 1995:
1488.
119. Busse WW. Rhinitis and asthma. In: Naclerio RM,
Durham SR, Mygind N, eds. Rhinitis mechanisms
and management. New York: Marcel Dekker, 1999:
435 45.
120. Bende M, Barrow I, Heptonstall J, et al. Changes in
human nasal mucosa during experimental coronavirus
common colds. Acta Otolaryngol (Stockh) 1989; 107:
2629.
121. Klimek L, Eggers G. Olfactory dysfunction in allergic
rhinitis is related to nasal eosinophilic inflammation. J
Allergy Clin Immunol 1997; 100: 158 64.
122. Andersson KE, Bende M. Adrenoceptors in the control of human nasal mucosal blood flow. Ann Otol
Rhinol Laryngol 1984; 93: 179 82.
123. Eccles R. Nasal airflow and decongestants. In: Naclerio RM, Durham SR, Mygind N, eds. Rhinitis mechanisms and management. New York: Marcel Dekker,
1999: 291 312.
124. Graf P, Juto JE. Sustained use of xylometazoline
nasal spray shortens the decongestive response and
induces rebound swelling. Rhinology 1995; 33: 147.
125. Morris S, Eccles R, Jawad MSJ, Riker DK, Witek TJ.
An evaluation of nasal response following different
treatment regimes of oxymetazoline with reference to
rebound congestion. Am J Rhinol 1997; 11: 10915.
126. Blue JA. Rhinitis medicamentosa. Ann Allerg 1968;
26: 425 9.
127. Toohill RJ, Lehman RH, Grossman TW, Belson TP.
Rhinitis medicamentosa. Laryngoscope 1981; 91:
1614 21.
128. Flanagan P, Eccles R. Physiological versus pharmacological decongestion of the nose in healthy human
subjects. Acta Otolaryngologica (Stockh) 1998; 118:
1103.
129. Howarth PH. Mediators of nasal blockage in allergic
rhinitis. Allergy 1997; 52: 12 8.
130. Doyle WJ, Boehm S, Skoner DP. Physiological responses to intranasal dose-response challenges with
histamine,
methacholine,
bradykinin,
and
prostaglandin in adult volunteers with and without
nasal allergy. J Allergy Clin Immunol 1990; 86: 924
35.
131. Vayonis AG, Seroky JT, Doyle WJ, Skoner DP,
Fireman P. Intranasal histamine, methacholine, and
bradykinin challenge in children with and without
allergy. Am J Rhinol 1995; 9: 1 7.
132. Shelton D, Eiser N. Histamine receptors in the human
nose. Clin Otolaryngol Allied Sci 1994; 19: 45 9.
133. Secher C, Kirkegaard J, Bprum P, et al. Significance
of H1 and H2 receptors in the human nose: rationale
for topical use of combined antihistamine preparations. J Allergy Clin Immunol 1982; 70: 211 8.
134. Eccles R, Wilson H. A kallikrein-like substance in cat
nasal secretion. Br J Pharmacol 1973; 49: 712 4.
135. Doyle WJ, Skoner DP, White M, et al. Pattern of
nasal secretions during experimental influenza virus
infection. Rhinology 1996; 34: 2 8.

Acta Otolaryngol 120

136. Proud D, Reynolds CJ, Lacapra S, et al. Nasal provocation with bradykinin induces symptoms of rhinitis
and a sore throat. Am Rev Respir Dis 1988; 173:
6136.
137. Rees GL, Eccles R. Sore throat following nasal and
oropharyngeal bradykinin challenge. Acta Otolaryngol (Stockh) 1994; 114: 3114.
138. Pongracic J, Naclerio R, Reynolds C, Proud D. A
competitive kinin receptor antagonist (DArg0, Hyp3,
DPhe7)-bradykinin, does not affect the response to
nasal provocation with bradykinin. Br J Pharmacol
1991; 31: 28794.
139. Mygind N, Naclerio RM. In: Naclerio RM, Durham
SR, Mygind N, eds. Rhinitis mechanisms and management. New York: Marcel Dekker, 1999: 221 56.
140. Schmidt BMW, Timmer W, Georgens AC, et al. The
new topical steroid ciclesonide is effective in the treatment of allergic rhinitis. J Clin Pharmacol 1999; 39:
10629.
141. Jones AS, Willatt DJ, Durham LM. Nasal airflow:
resistance and sensation. J Laryngol Otol 1989; 103:
90911.
142. Yaniv E, Hadar T, Shvero J, Raveh E. Objective and
subjective nasal airflow. Am J Otolaryngol 1997; 18:
2932.

Nasal airflow in health and disease

595

143. Eccles R. The relationship between subjective and

objective measures of nasal function. Jpn J Rhinol
1998; 37: 61 9.
144. Sipila J, Suonpaa J. A prospective study using rhinomanometry and patient clinical satisfaction to determine if objective measurements of nasal airway
resistance can improve the quality of septoplasty. Eur
Arch Otorhinolaryngol 1997; 254: 387 90.
145. McCaffrey TV. Rhinomanometry and diagnosis
of nasal obstruction. Fac Plast Surg 1990; 7: 266
73.
Submitted April 25, 2000; accepted April 27, 2000
Address for correspondence:
Ronald Eccles
Common Cold Centre
Cardiff School of Biosciences
Cardiff University
Cardiff CF1 3US
UK
Tel.: + 44 29 2087 4099
Fax: + 44 29 2087 4093
E-mail: eccles@cardiff.ac.uk