EFFECTS OF ETOMIDATE AND HYPOTHERMIA ON CEREBRAL METABOLISM AND BLOOD-FLOW IN A CANINE MODEL OF HYPOPERFUSION

Citation
Rt. Frizzell et al., EFFECTS OF ETOMIDATE AND HYPOTHERMIA ON CEREBRAL METABOLISM AND BLOOD-FLOW IN A CANINE MODEL OF HYPOPERFUSION, Journal of neurosurgical anesthesiology, 5(2), 1993, pp. 104-110
Citations number
25
ISSN journal
08984921
Volume
5
Issue
2
Year of publication
1993
Pages
104 - 110
Database
ISI
SICI code
0898-4921(1993)5:2<104:EOEAHO>2.0.ZU;2-B
Abstract
Etomidate is a nonbarbiturate hypnotic agent which, like the barbitura tes, decreases the cerebral metabolic rate of oxygen consumption (CMRO 2) 35-50%. The present studies assessed whether etomidate decreased CM RO2 through temperature-dependent mechanisms and whether the combinati on of etomidate and moderate hypothermia (28-degrees-C) decreased CMRO 2 more than hypothermia alone. Nineteen anesthetized dogs were treated with saline etomidate (burst-suppressive doses), etomidate with hypot hermia, or hypothermia alone. Etomidate did not affect (p > 0.05) the mean arterial pressure (MAP, mm Hg) but modestly lowered the heart rat e [HR; 124 +/- 6 to 105 +/- 14, (mean +/- SEM); p < 0.05] whereas hypo thermia (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 administrat ion did not result in a change (p > 0.05) in the esophageal, brain par enchymal, or subdural temperature. CMRO2 (Ml/100 g/min) decreased (p < 0.05) during etomidate administration (3.2 +/- 0.4 to 1.7 +/- 0.2) an d hypothermia (3.5 +/- 0.2 to 1.1 +/- 0.2), but the addition of etomid ate to hypothermia did not further reduce CMRO2 in the animals (3.1 +/ - 0.5 to 1.3 +/- 0.2) despite decreasing their brain hemispheric elect rical activity from 9 +/- 1 Hz to a burst-suppressive state. During hy potension (MAP 30 +/- 2) induced by sodium nitroprusside and trimethap han administration, the cerebral arteriovenous difference in O2 (AVDO2 ) increased (p < 0.05) in the saline group (5.4 +/- 0.9 to 10.7 +/- 1. 0 ml/dl) but not in the other groups. Thus, etomidate does not have ad verse cardiovascular effects associated with moderate hypothermia, and decreases CMRO2 independently of brain temperature changes. Etomidate , however, in this model does not further reduce CMRO2 in moderately h ypothermic animals despite decreasing their brain hemispheric electric al activity. Etomidate, hypothermia, and the combination of etomidate and hypothermia all blunt the hypotension-induced increase in cerebral AVDO2.