Abstract

Because propofol has cerebral effects similar to those observed for barbiturates, we postulated that it too might offer protection against a focal cerebral ischemic insult. Spontaneously hypertensive male rats were anesthetized with halothane (in 50% O2/balance N2), and their tracheas were intubated and their lungs mechanically ventilated. A right subtemporal craniectomy was performed and a 10-0 suture placed around the middle cerebral artery. Rats were then randomly assigned to one of two anesthetic groups. In one half of the rats (n = 14), the inspired halothane concentration was reduced to 0.5-0.7%. In the remainder (n = 14), halothane was discontinued, and an intravenous infusion of 1% propofol was given in doses sufficient to produce and maintain electroencephalographic burst suppression. The middle cerebral artery was then reversibly ligated for 2 h while pericranial temperature was maintained at 37.0 +/- 0.1 degrees C (mean +/- SD). After the ligature was removed and reperfusion confirmed, all rats were allowed to recover for 96 h. Neurologic evaluations were performed at both 24 and 96 h postischemia. The rats were then killed and the brains removed, frozen, sectioned, and stained with nitro blue tetrazolium. Infarct volume was determined by computerized planimetry. Physiologic values were similar between anesthetic groups, although plasma glucose was significantly greater during ischemia in the halothane group (125 +/- 25 vs. 83 +/- 8 mg/dl, P less than 0.001). At both 24 and 96 h postischemia, neurologic deficits were mild but without a difference between groups. Neurologic scores at 96 h postischemia correlated with cerebral infarct volume (r = 0.49, P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)