Cerebral protective effects of etomidate: experimental and clinical aspects

Abstract

Reduction of cerebral blood flow below a critical threshold for a protracted time interval results in irreversible metabolic events culminating in cell death. The development of agents capable of extending the tolerable ischemic interval is of great importance as such agents may allow time for therapeutic measures to be accomplished which could restore cerebral perfusion. This issue is of particular pertinence in the treatment of complex cerebrovascular diseases when local (or global) cerebral blood flow must be interrupted during vascular reconstruction. Thiopental achieved great popularity once protective properties were demonstrated experimentally. Unfortunately, serious cardiovascular depression associated with high-dose barbiturates as well as prolonged duration of action may decrease collateral flow and limit their utility. Etomidate is a nonbarbiturate carboxylated imidazole which is capable of similar cerebral metabolic suppression without significant cardiac side effects. Accumulating experimental evidence supports the protective properties of this drug and suggests that it may be valuable clinically for this purpose. Significant adrenal suppression is a major toxic effect that must be treated if large doses or protracted administration is planned.