Mechanisms of Cerebrovascular Dilation by Ether in Monkeys

We hypothesized that when the depth of ether anesthesia is increased from 2 to 5%, cerebral vessels dilate secondary to circulating catecholamine stimulation of cerebral metabolism. Cerebral blood flow (CBF) by 133 Xe clearance and cerebral metabolic rate for oxygen (CMRO 2 ) were measured on 2% and then 5% ether in air in two groups of seven monkeys each during mechanical ventilation. Propranolol, 0.5 mg/kg i. v., was infused over 5 min in one group, and the other received saline. All measurements were repeated on 5% and 2% ether. Cerebrovascular resistance (CVR) fell by 30%, from 2.28 2± 0.61 (mean ± SD) to 1.51± 0.28 mm Hg ml −1 100 g −1 min −1 (p < 0.01), with the increase in ether from 2 to 5%. CBF and CMRO 2 were unaltered from values of about 45 ml 100 g −1 min −1 and 2.3 ml 100 g −1 min −1 , respectively. During 5% ether anesthesia, propranolol had no effect on CBF, CMRO 2 , or CVR. On 2% ether, it increased CVR twofold, from 1.5 ± 0.30 to 3.0 ± 1.0 mm Hg ml −1 100 g −1 min −1 , and decreased CBF by 33%, from 48 ± 8 to 32 ± 10 ml 100 g −1 min −1 . Plasma epinephrine was twofold higher on 2% compared to 5% ether, both before and after saline or propranolol infusion. In monkeys, cerebrovascular dilation by ether at 5% compared to 2% is not secondary to catecholamine stimulation of CMRO 2 . It may result from a direct effect of either plasma catecholamines or ether on the cerebrovasculature.