Regulation of cerebral blood flow in atherosclerotic monkeys

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Abstract
Effects of atherosclerosis on cerebral vascular responses of 9 normal and 8 atherosclerotic, anesthetized, cynomolgous monkeys to hypercapnia and hypotension were studied. After 20 mo. of an atherogenic diet, the common carotid and internal carotid arteries had fibrofatty lesions with some necrosis and calcification, and intracranial arteries had only fatty streak changes. Base-line cerebral blood flow (measured with microspheres) and vascular resistance were similar in the normal and atherosclerotic monkeys. Despite significant obstruction of large extracranial arteries by atherosclerotic lesions, distal vessels dilated to maintain flow normal. Reduction of mean arterial pressure to 51 .+-. 7 mmHg in atherosclerotic monkeys and 42 .+-. 4 mmHg in normal monkeys did not decrease cerebral flow because cerebral vessels dilated to maintain flow constant. Cerebral vasodilator responses to hypercapnia were impaired by atherosclerosis. Cerebral blood flow increased from 40 .+-. 6 (mean .+-. SE) to 190 .+-. 17 ml .cntdot. min-1 .cntdot. 100 g-1 during hypercapnia (PaCO2 [arterial partial pressure of CO2] = 64 mmHg) in normal monkeys and from 34 .+-. 2 to 99 .+-. 20 ml/min (PaCO2 = 65 mmHg) in atherosclerotic monkeys. Measurement of regional blood flow indicated that dilator responses in atherosclerotic monkeys were impaired in cerebral gray and white matter, cerebellum and brain stem. In a primate model of atherosclerosis, maximal cerebral vasodilator responses to hypercapnia are impaired, but during a less pronounced vasodilator stimulus autoregulatory responses to hypotension are perserved.