Mechanisms of Cerebrovascular Dilation by Ether in Monkeys

• Published in: Journal of cerebral blood flow and metabolism 1987-04, Vol.7 (2), p.230-236
• Main Authors: Kang, Yoo Goo, Nemoto, Edwin M., Bleyaert, Achiel L., Winter, Peter M., Eidelman, Benjamin H., Taylor, Floyd H.
• Format: Article
• Language: English
• Subjects: Anesthetics. Neuromuscular blocking agents; Animals; Biological and medical sciences; Brain - metabolism; Catecholamines - pharmacology; Cerebrovascular Circulation; Ether - pharmacology; Ethyl Ethers - pharmacology; Macaca fascicularis; Male; Medical sciences; Neuropharmacology; Oxygen Consumption; Pharmacology. Drug treatments; Propranolol - pharmacology; Vasodilation - drug effects
• ISSN: 0271-678X; 1559-7016
• DOI: 10.1038/jcbfm.1987.48

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 133Xe clearance and cerebral metabolic rate for oxygen (CMRO2) 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 CMRO2 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, CMRO2, 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 CMRO2. It may result from a direct effect of either plasma catecholamines or ether on the cerebrovasculature.