We have found that anesthetic technique modifies the neurological and pathological sequelae of unilateral middle cerebral artery and internal carotid artery occlusion in dogs. Occlusion was performed in seven groups of six dogs during each of the following anesthetic regimens: light (0.8%) halothane, “awake,” deep (1.9%) halothane, deep halothane with mean arterial pressure reduced to 55 torr, pentobarbital (56 mg per kilogram), light halothane plus 40 mg per kilogram thiopental begun just before cerebral artery occlusion, and light halothane plus 40 mg per kilogram thiopental begun 15 minutes after occlusion. Body temperature, arterial Pco2Po2pH, and blood pressure (except as noted above) were maintained normal. Neurological examinations were performed daily. On the seventh day the dogs were killed and their brains removed for pathological study. Hemiparesis occurred in five of six dogs under light halothane and five of six awake dogs; a mean of 10.8% and 9.6%, respectively, of their right hemispheres were infarcted. In the deep halothane groups, all of the normotensive and five of the six hypotensive dogs became severely hemiplegic; mean infarction size was 28.2% and 34.1%, respectively. Only one of the 18 dogs who received a barbiturate sustained a neurological deficit — a transient unilateral weakness. Means of 1.4%, 2.7%, and 0.1% of the right hemisphere were infarcted in the barbiturate animals. The protective action of barbiturates in canine acute focal cerebral ischemia suggests that they should be considered for anesthesia in surgery requiring cerebral vessel occlusion and perhaps even for treatment of acute stroke.