Active Hyperemia

Active hyperemia is the increase in organ blood flow (hyperemia) that is associated with
increased metabolic activity of an organ or tissue. An example of active hyperemia is the
increase in blood flow that accompaniesmuscle contraction, which is also called exercise
or functional hyperemiain skeletal muscle. Blood flow increases because the increased
oxygen consumption of during muscle contraction stimulates the production of vasoactive
substances that dilate the resistance vessels in the skeletal muscle. Other examples include
the increase in gastrointestinal blood flow during digestion of food, the increase in coronary
blood flow when heart rate is increased, and the increase in cerebral blood flow associated
with increased neuronal activity in the brain. The figure shows that there is a resting flow
associated with the basal oxygen consumption of the tissue. As the oxygen consumption
increases, there is generally a near-linear increase in blood flow until the vessels begin to
achieve a maximally dilated state.
The magnitude of active hyperemia responses differ among organs because of the relative
changes in metabolic activity from rest and their vasodilatory capacity. Active hyperemia
can result in up to a 50-fold increase in muscle blood flow with maximal exercise, whereas
cerebral blood flow may only increase 2-fold with increased neuronal activity.
Active hyperemia can also be influenced by competing vasoconstrictor mechanisms. For
example, sympathetic activationduring exercise can reduce the maximal skeletal muscle
active hyperemia compared to what would occur in the absence of sympathetic activation.
Active hyperemia may be due to a combination of tissue hypoxia and the generation of
vasodilator metabolites such aspotassium ion, carbon dioxide, nitric oxide, and adenosine.
Revised 03/28/2007
http://ocw.tufts.edu/data/51/561424/561434_xlarge.jpg

Reactive Hyperemia
Reactive hyperemia is the transient increase in organ blood flow that occurs following a
brief period of ischemia (e.g., arterial occlusion). Reactive hyperemia occurs following the
removal of a tourniquet, unclamping an artery during surgery, or restoring flow to a coronary
artery after recanalization (reopening a closed artery using an angioplasty balloon or clot
dissolving drug).In general, the ability of an organ to display reactive hyperemia is similar to
its ability to displayautoregulation.
In the following figure, the left panel shows the effects of a 2 min arterial occlusion on blood
flow. In this example, blood flow goes to zero during arterial occlusion. When the occlusion
is released, blood flow rapidly increases (i.e., hyperemia occurs) that lasts for several
minutes. The hyperemia occurs because during the period of occlusion, tissue hypoxia and
a build up of vasodilator metabolites (e.g., adenosine) dilate arterioles and decrease
vascular resistance. Then when perfusion pressure is restored (i.e., occlusion released),
flow becomes elevated because of the reduced vascular resistance. During the hyperemia,
the tissue becomes reoxygenated and vasodilator metabolites are washed out of the
tissue. This causes the resistance vessels to regain their normal vascular tone, thereby
returning flow to control. The longer the period of occlusion, the greater the metabolic
stimulus for vasodilation leading to increases in peak reactive hyperemia and duration of
hyperemia. Depending upon the organ, maximal vasodilation as indicated by peak flow,
may occur following less than one minute (e.g., coronary circulation) of complete arterial
occlusion, or may require several minutes of occlusion (gastrointestinal
circulation). Myogenic mechanisms may also contribute to reactive hyperemia in some
tissues. By this mechanism, arterial occlusion results in a decrease in pressure downstream
in arterioles, which can lead to myogenic-mediated vasodilation.