This study examined the effect of prolonged postischemic halothane administration on outcome from transient focal cerebral ischemia in rats. Conscious normothermic rats were subjected to 75 minutes of filament middle cerebral artery occlusion (MCAO). Animals were then divided into two groups. The Awake group (n = 15) remained awake following ischemia. The Halothane group (n = 15) received 1.3-1.4% halothane for 5 hours after onset of recirculation. In both groups, brain temperature was maintained at 37.5 degrees C during ischemia and the first 22 hours of recovery. Seven days after ischemia, the severity of hemiparesis and cerebral infarct size were examined. Neurologic scores did not differ between groups (Awake = 1+/-2.75; Halothane = 2+/-2; p = 0.772, median +/- interquartile range). Neurologic scores and total infarct volumes were correlated (R = 0.653; p = 0.0004). Cortical (Awake = 76+/-57 mm3; Halothane = 90+/-57 mm3; p = 0.494, mean +/- standard deviation), subcortical (Awake = 71+/-33 mm3; Halothane = 80+/-35 mm3; p = 0.472), and total (Awake = 147+/-88 mm3; Halothane = 171+/-91 mm3; p = 0.477) infarct volumes were not significantly different between groups. The data indicate that postischemic halothane administration offers no benefit in ameliorating damage from focal cerebral ischemia. This suggests that the neuroprotective effect of halothane observed in other studies is consistent with influences on intra-ischemic pathophysiology only.