Frizzell R T, Fichtel F M, Jordan M B, Weprin B E, Borchers D J, Allen E C, Pogue W R, Batjer H H
Department of Neurological Surgery, University of Texas Southwestern Medical Center, Dallas 75235-8855.
J Neurosurg Anesthesiol. 1993 Apr;5(2):104-10. doi: 10.1097/00008506-199304000-00006.
Etomidate is a nonbarbiturate hypnotic agent which, like the barbiturates, decreases the cerebral metabolic rate of oxygen consumption (CMRO2) 35-50%. The present studies assessed whether etomidate decreased CMRO2 through temperature-dependent mechanisms and whether the combination of etomidate and moderate hypothermia (28 degrees C) decreased CMRO2 more than hypothermia alone. Nineteen anesthetized dogs were treated with saline, etomidate (burst-suppressive doses), etomidate with hypothermia, or hypothermia alone. Etomidate did not affect (p > 0.05) the mean arterial pressure (MAP, mm Hg) but modestly lowered the heart rate [HR; 124 +/- 6 to 105 +/- 14, (mean +/- SEM); p < 0.05] whereas hypothermia (without or with etomidate) lowered (p < 0.05) both MAP (141 +/- 4 to 116 +/- 5 and 135 +/- 6 to 81 +/- 7) and HR (135 +/- 14 to 84 +/- 3 and 135 +/- 10 to 69 +/- 5, respectively). Etomidate administration did not result in a change (p > 0.05) in the esophageal, brain parenchymal, or subdural temperature. CMRO2 (ml/100 g/min) decreased (p < 0.05) during etomidate administration (3.2 +/- 0.4 to 1.7 +/- 0.2) and hypothermia (3.5 +/- 0.2 to 1.1 +/- 0.2), but the addition of etomidate to hypothermia did not further reduce CMRO2 in the animals (3.1 +/- 0.5 to 1.3 +/- 0.2) despite decreasing their brain hemispheric electrical activity from 9 +/- 1 Hz to a burst-suppressive state.(ABSTRACT TRUNCATED AT 250 WORDS)
