Cerebral Circulatory and Metabolic Responses to Intravenously Administered Lorazepam

Abstract

Cerebral vascular and metabolic effects of lorazepam were evaluated in 10 awake monkeys (Macaca fascicularis) by a modification of the Kety-Schmidt technique; 5 received ketamine, 10 mg/kg, i.m., 5-8 h prior to the study, but all animals were otherwise treated identically. Monkeys receiving ketamine had significantly greater (P < 0.05) cerebral blood flow (CBF) values before lorazepam was given (46 .+-. 1 ml/100 g per min) than did monkeys not receiving ketamine (41 .+-. 1 ml/100 g per min), but in all other respects, premedicated and unpremedicated animals did not differ. Lorazepam administration did not significantly alter systemic arterial blood pressure or blood-gas values. It did decrease CBF by 26% and increase cerebral vascular resistance (CVR) by .apprx. 25% (P < 0.01). The cerebral metabolic rate for glucose (CMRg) decreased 42% (P < 0.05). Following lorazepam administration, the cerebral metabolic rate for oxygen (CMRO2) decreased by 21-30%. When combined CMRO2 data for the 2 anesthetic groups are pooled, this decrease is significant (P < 0.05). Sedative doses of lorazepam decrease cerebral blood flow and metabolism with minimal effects on blood pressure and blood-gas values. Lorazepam administration did not produce any change in cerebral metabolism indicative of brain hypoxia or ischemia.