Cardiovascular and cerebrovascular effects of isoflurane-induced hypotension in the baboon.

Mean arterial pressure (MAP) decreased by 10, 20, 40, and 50% of its baseline value in six anesthetized baboons with the administration of increasing concentrations of isoflurane. Mean arterial pressure, right atrial pressure, pulmonary artery pressures, and cardiac output were measured at each decrement in arterial pressure, and after the withdrawal of the isoflurane. At the same times, cerebral blood flow, the cerebral metabolic rate for oxygen, and the cerebral metabolic rate for glucose were determined. Cerebrovascular reactivity was assessed before, during, and after the administration of isoflurane, and morphologic evidence of ischemic cell change was sought at the end of the investigation. Isoflurane produced dose-related decreases in systemic vascular resistance and MAP; heart rate, cardiac output, and stroke volume did not change significantly. Although cerebral metabolism was depressed in a dose-related manner, the response of the cerebral blood flow (CBF) was biphasic. At low isoflurane concentrations, CBF decreased significantly and then increased to reach baseline values at the highest concentration. Cerebrovascular reactivity was intact at baseline and at the 20% decrement in MAP; it was impaired at the 50% decrease in MAP and when studied 100 min after the withdrawal of isoflurane. There was no morphologic evidence of ischemic cell damage in any animal.