neuronal activity in specific brain regions lead
to increases in blood flow to those regions.
The brain shows excellent autoregulation
between MAPs of about 60 and 130 mm Hg
(Fig. 7.11). This is important because cerebral
function relies on a steady supply of oxygen
and cannot afford to be subjected to a reduc-
tion in flow caused by a fall in arterial pres-
sure. If MAP falls below 60 mm Hg, cerebral
perfusion becomes impaired, which results in
depressed neuronal function, mental confu-
sion, and loss of consciousness. When arte-
rial pressure is above the autoregulatory range
(e.g., in a hypertensive crisis), blood flow and
pressures within the cerebral microcirculation
increase. This may cause endothelial and vas-
cular damage, disruption of the blood-brain
barrier, and hemorrhagic stroke. With chronic
hypertension, the autoregulatory curve shifts
to the right (see Fig. 7.11), which helps to pro-
tect the brain at higher arterial pressures. How-
ever, this rightward shift then makes the brain
more susceptible to reduced perfusion when
arterial pressure falls below the lower end of
the rightward-shifted autoregulatory range.
Local metabolic mechanisms play a domi-
nant role in the control of cerebral blood flow.
Considerable evidence indicates that changes
in carbon dioxide are important for coupling
Perfusion Pressure (mm Hg)
■ FIGURE 7.11 Autoregulation of cerebral blood
flow. Cerebral blood flow shows excellent autoreg-
ulation between MAPs of 60 and 130 mm Hg.
The autoregulatory curve shifts to the right with
chronic hypertension or acute sym pathetic activa-
tion. This shift helps to protect the brain from the
damaging effects of elevated pressure.
tissue metabolism and blood flow. Increased
oxidative metabolism increases carbon diox-
ide production, which causes vasodilation. It
is thought that the carbon dioxide diffuses into
the cerebrospinal fluid, where hydrogen ion is
formed by the action of carbonic anhydrase;
the hydrogen ion then causes vasodilation. In
addition, carbon dioxide and hydrogen ion
increase when perfusion is reduced because
of impaired washout of carbon dioxide. Aden-
osine, nitric oxide, potassium ion, and myo-
genic mechanisms have also been implicated
in the local regulation of cerebral blood flow.
Cerebral blood flow is strongly influenced
by the partial pressure of carbon dioxide and,
to a lesser extent, oxygen in the arterial blood
(Fig. 7.12). Cerebral blood flow is highly sen-
sitive to small changes in arterial partial pres-
sure of CO2 (PCO2) from its normal value of
about 40 mm Hg, with increased PCO2 (hyper-
capnia) causing pronounced vasodilation and
decreased PCO2 (hypocapnia) causing vaso-
to be
responsible for the changes in vascular resist-
ance when changes occur in arterial PCO2.
The importance of CO2 in regulating cerebral
blood flow can be demonstrated when a per-
son hyperventilates, which decreases arterial
PCO2. W hen this occurs, a person becomes
“light headed” as the reduced PCO2 causes
cerebral blood flow to decrease. Severe arte-
rial hypoxia (hypoxemia) increases cerebral
blood flow. Arterial PO2 is normally about 95
to 100 mm Hg. If the PO2 falls below 50 mm
Hg (severe arterial hypoxia), it elicits a strong
helps to maintain oxygen delivery despite
the reduction in arterial oxygen content. As
described in Chapter 6, decreased arterial
PO2 and increased PCO2 stimulate chemore-
ceptors, which activate sympathetic efferents
to the systemic vasculature to cause vaso-
constriction; however, the direct effects of
hypoxia and hypercapnia override the weak
effects of sympathetic activation in the brain
so that cerebral vasodilation occurs and oxy-
gen delivery is enhanced.
larger cerebral vessels, activation of these nerves
has relatively little influence on cerebral blood
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