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ernia

and diabetes fnellitus (1).

and atheroscleroservations the prevalence of smoking and mortality from coromry heart disease
have declined, but 25% of all ~~~~~~v~s~~lar
deaths in the
developed countries are still attributable to cigarette smoking (3). Even in countries where the incidence of coronary
heart disease is relatively low, smoking shows

From the Departmentof Pharmacology,Divisionof ClinicalPharmacologyand Departmentsof Biophysicsand Physiology,CardiovascularResearch


Institute Maastricht,University of Limbuq, Maastricht,The Netherlands.
Manuscriptreceived March29, 1993;revised manuscriptreceived.iarne
1%
I Dr. M. J. F. Kool, Deparwnt of Pharmacology, University of Limburg, P. 0. Box 616, 6209 MD Maastricht,The
Netherlands.
81993 by

the AmericanColtegeof Cardiology

1. DemographicDatafor Smokersand Nonsmokers

Gender
Ageiyr)
Weight
(kg)
He&%(cm)
BU (m3,

Smokers
(n = 14)

Nonsmokers
(n = 14)

9Ml5F
37 (25-W
73 (55-88)
175(158-186)
1.9(M-2.1)

9M;SF
37(w-541
72 (52-931
174(161-183)
1.9(1.6-2.0)

Vahwsin prcnthesesareran@s.BSA = body surfacearea, calculated


accord&~to tie fomwh of Ih Boisand Du Bois (14).

the left arm. Pulse pressure (AP) was ~efi~cd as ~y~to~~c


minus diastolic blood pressure.

bit& smokers (study 1). In addition, these!v


were compared with those in ~n~~~~~~~ subjects (study 2).

arm at heart level. The


whole arm was deiced in an incubator to keep c~vironm~ntal
nstant (28C).In addition, the skin temperay a skin electrode thermomrature was similar before and

E&C common carotid

bl

every mmute. In addition, cardiac


flowwere determined before and

strain gauge, represent total (cutaneous and muscle) forearm


blood flow. Hand circulation was eliminated by inflating a
wrist cuff to suprasystolic pressure (220mm Hg) for 4 min.

Figure 1. The short-term effec of


smokingon vessel wall properties
of large arteries before (open bsrs)
and after (solid bars) smokingone
cigarette. Data are mean value -1SEM. *p c Q.05,**p < 0.01(diqerence between period before and after smoking).BA = brachialartery;
= complhce
coeficient;
::* = common carotid artery;
D = diameter; DC = distensibility
coefkient.

KWL EKAL.

SMOKING AND AKIERIAL WALL PROPERTIES

3.

HemodynamicIMa for Smokers and Nonsmokers


Smokers

bighsic s&33, At low doses

Nonsmokers

of smoking can be explained by the ~~cot~~e~~~d~cc~


sympathetic activation. Nicotine induces t e release of both
epinephrine and ~orep~~e~bri~~,
thetic nerve activity has been
), the increase in plas
cts stimulation of the adre
peripheral mecba~~sms(e
nephrine clearance) (18)+The net
dependlenton the mixed
nephrine at the d~er~~t

it causes
medulla awd an
d

stimulation or direct

in these studies the increment in


is lower than the incrczss in heart
se short-term hemodynamiceffects

After a 4-h noasmoking period, heart rate at rest was


higher in habitual smokers than in nons~~lokers.This differcace could not be explained lay differences in physical
activity level in the two groups because, on average, smokers and nonsmokers beloved the same daily work and
s activatorswere comparabk. In previous studies,
smokers (26)the heart rate has been persistently
could to be elevated
of withdrawal phenomenon.
rs in our
study was not different from that in nonsmokers. Other
studies have been inconsistent with regard to blood pressure
in habitual smokers. Overall (X,27), casual as well as
ambulatory blood pressure values in habitual smokers have

2.
3.

om mtional vitsnlstatistics.
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discasf:
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II.

function and kemostasis (20,34,35).


In addition, according to the current view of atherosclerotic disease, plaque ruptun is an important feature. Pt has
been demonstrated that most of the acute coronary syndromes are due to the disruption of small, nonstenotic
plaques (36). These small plaques are generally not detected
with the present diagnostic techniques and might already be
present in young smokers (36). Increased arterial wall stiffness, increased blood pressure ad a bigher heart rate are
short-term effects of smdhg that enhance the load on the
site. sf ~t~~~osc~e~ot~~
vessel wall. In addition, at t
plaques, the distribution of circu rential and tensile stress
is altered, which might further increase the load at the plaque
(37).The smoking-induced increased load at the atherosclerotic plaque may induce plaque rupture and lead to acute
ischemic events.

12.

13.
14.
15.

16.

Van Bortel LM. Hocks AFG, Kool MJF, ~~~~k~r~~o~dier


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3!%?;324:242-50.
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the
distensibility of superficial wrterics. Witrasound f&d Biol I99%16:121-8.
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area if height and weight be known. Arch Intern Med 19f6;17%93=71.
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marI
Taylor P. Ganglionic siirldihg
and blocking agents. In:
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of

17. Care CG, Lever MJ, Parker M-L Fish Pd. EfTtxt of eiga
the pattern of arterial bb3d flow: postiiblc insight i
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IAl
l992:A14:251-MI.
19. Berlin I, Cournot A, Renout P, Duchier J, S&W

KOOL ET AL..
SMOKING
AND ARTERK AL WALL

PROPERTIES

namic effects of smokingin babituai smokers. A methodological study.


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and local cold test: rno~~olog~c~~


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