Cerebral circulatory and metabolic responses to intravenously administered lorazepam

Cerebral vascular and metabolic effects of lorazepam were evaluated in ten awake monkeys by use of a modification of the Kety-Schmidt technique. Five received ketamine, 10 mg/kg, im, five to eight hours 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/min) than did monkeys not receiving ketamine (41 +/- 1 ml/100 g/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. However, it did decrease CBF by 26 per cent and increase cerebral vascular resistance (CVR) by approximately 25 per cent (P < 0.01). The cerebral metabolic rate for glucose (CMRg) decreased 42 per cent (P < 0.05). Following lorazepam administration, the cerebral metabolic rate for oxygen (CMRO2) decreased by 21-30 per cent. When combined CMRO2 data for the two anesthetic groups are pooled, this decrease is significant (P < 0.05). This study indicates that 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.