156
CARDIOVASCULAR PHYSIOLOGY CONCEPTS
Reactive and Active Hyperemia
Reactive hyperemia is the transient increase in
organ blood flow that occurs following a brief
period of ischemia, usually produced by tem-
porary arterial occlusion
.
Figure 7.4 shows
the effects of a 2-minute arterial occlusion
on blood flow. During the occlusion period,
blood flow goes to zero. W hen the occlusion
is released, blood flow rapidly increases above
normal levels (hyperemia) that lasts for sev-
eral minutes. In most tissues, experiments
have suggested that the hyperemia occurs
because during the occlusion period, tissue
hypoxia and a buildup of vasoactive metabo-
lites relax the smooth muscle of precapillary
resistance vessels.
W hen the
occlusion is
released and perfusion pressure is restored,
flow becomes elevated because of the reduced
vascular resistance. During the hyperemia,
oxygen becomes replenished and vasodilator
metabolites are washed out of the tissue, caus-
ing the resistance vessels to regain their nor-
mal vascular tone and thereby return flow to
normal levels. The longer the period of occlu-
sion, the greater the metabolic stimulus for
vasodilation, leading to increases in peak flow
and duration of hyperemia. Maximal vasodi-
lation, as indicated by a maximal peak hyper-
emic flow, may occur following <1 minute of
complete arterial occlusion, or it may require
several minutes of occlusion depending on
Time (min)
■ FIGURE 7.4 Reactive hyperemia. Arterial occlu-
sion (no flow ) for 2 minutes followed by reperfu-
sion results in a transient increase in blood flow
(reactive hyperemia). The m agnitude and duration
of the reactive hyperemia are directly related to
the duration of ischemia.
the vascular bed and its metabolic activity.
For example, in the beating heart (high meta-
bolic activity), maximal reactive hyperemic
responses are seen with coronary occlusions
of <1 minute, whereas in resting skeletal mus-
cle (low metabolic activity), several minutes
of ischemia are necessary to elicit a maximal
vasodilator response. Myogenic mechanisms
may also contribute to reactive hyperemia
in some tissues because arterial occlusion
decreases the pressure in arterioles, which can
lead to myogenic-mediated vasodilation.
Several
examples
of reactive
hyperemia
exist. The application of a tourniquet to a limb,
and then its removal, results in reactive hyper-
emia. During surgery, arterial vessels are often
clamped for a period of time; release of the
arterial clamp results in reactive hyperemia.
Transient coronary artery occlusions (e.g., cor-
onary vasospasm) result in subsequent reactive
hyperemia within the myocardium supplied by
the coronary vessel.
Active hyperemia is the increase in organ
blood flow that is associated with increased
metabolic activity of an organ or tissue
.
With
increased metabolic activity, vascular resist-
ance decreases owing to vasodilation and
vascular recruitment (particularly in skeletal
muscle). Active hyperemia occurs during mus-
cle contraction (also termed exercise or func-
tional hyperemia), increased cardiac activity,
increased mental activity, and increased gas-
trointestinal activity during food absorption.
In Figure 7.5, the left panel shows the
effects of increasing tissue metabolism for
2 minutes on mean blood flow in a rhythmi-
cally contracting skeletal muscle. Within sec-
onds of initiating contraction and the increase
in metabolic activity, blood flow increases. The
vasodilation is thought to be caused by a com-
bination of tissue hypoxia and the generation
of vasodilator metabolites such as potassium
ion, carbon dioxide, nitric oxide, and adeno-
sine. This increased blood flow (i.e., hyper-
emia) is maintained throughout the period of
increased metabolic activity and then subsides
after contractions cease and normal metabo-
lism is restored. The amplitude of the active
hyperemia is closely related to the increase in
metabolic activity (e.g., oxygen consumption)
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