Cerebral Circulation

Under resting conditions, blood flow to the brain is about 50 mL/min per 100 g, accounting for about 15%

of cardiac output. O2 consumption by the human brain averages about 3.5 mL/min per 100 g. Gray matter has a very high rate of oxidative metabolism and its flow rate is up to six times higher than that of white matter. The brain, particularly gray matter, is exquisitely sensitive to hypoxia and consciousness is lost in humans after as little as 10 min of ischemia, with irreversible cell damage occurring within minutes. Thus, the primary function of the cerebral circulation is to ensure an uninterrupted supply of O2 to the brain.

As in the coronary circulation, cerebral resistance vessels are predominantly under the control of intrinsic factors. Cerebral arterioles respond with dilation to increases in metabolic activity in the brain. Cerebral blood flow falls when brain function and metabolism are reduced during sleep or anesthesia. Any increase in metabolism in a specific area of the brain will result in an increased blood flow to that region. Unlike any other organ, the brain is able to safeguard its own blood supply by controlling the vascular resistance of other organs through its autonomic outflow. Even though sympathetic nerves can be demonstrated on the cerebral blood vessels, the constrictor response to stimulation of these nerves is weak, presumably reflecting a low density of adrenergic receptors on cerebral arterioles. Parasym-pathetic stimulation exerts a similarly weak vasodilatory response in the brain. The cerebral vessels also respond poorly to blood-borne vasoactive agents because of the highly restrictive nature of cerebral capillaries. This functional adaptation of the cerebral microvasculature is called the blood-brain barrier. Although O2 and CO2 readily cross the blood-brain barrier, glucose (the primary energy source for the brain) and amino acids use bidirectional transport systems in the endothelium of cerebral capillaries.

Pressure flow autoregulation is well developed in the brain, which maintains a normal cerebral blood flow at arterial pressures between 60 and 140 mm Hg. This autoregulatory range is shifted to the right (blood flow maintained constant over a range of higher pressures) by chronic arterial hypertension and during acute sympathetic stimulation. Both metabolic and myogenic mechanisms have been implicated in cerebral autoregulation. Unlike the heart, however, cerebral arterioles appear to be more sensitive to changes in arterial blood PCO2 than to changes in PO2. Figure 7 shows that even a slight elevation in arterial PCO2 (hypercapnia) is accompanied by a large increase in cerebral blood flow. This observation has led to the proposal that CO2 is an important metabolite that mediates intrinsic blood flow regulation in the brain. The vasoactive effects of CO2 have been attributed to its effect on tissue pH (increased PCO2 leads to a reduced pH). Indeed, the hypercapnic vasodilation seen in the brain is considered to be a

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