Effects of postischemic halothane administration on outcome from transientfocal cerebral ischemia in the rat

This study examined the effect of prolonged postischemic halothane administ ration 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 Aw ake group (n = 15) remained awake following ischemia. The Halothane group ( n = 15) received 1.3-1.4% halothane for 5 hours after onset of recirculatio n. In both groups, brain temperature was maintained at 37.5 degrees C durin g ischemia and the first 22 hours of recovery. Seven days after ischemia, t he severity of hemiparesis and cerebral infarct size were examined. Neurolo gic scores did not differ between groups (Awake = 1 +/- 2.75; Halothane = 2 +/- 2; p = 0.772, median +/- interquartile range). Neurologic scores and t otal infarct volumes were correlated (R = 0.653; p = 0.0004). Cortical (Awa ke = 76 +/- 57 mm(3); Halothane = 90 +/-: 57 mm(3),p = 0.494, mean +/- stan dard deviation), subcortical (Awake = 71 +/- 33 mm(3); Halothane = 80 +/- 3 5 mm(3); p = 0.472), and total (Awake = 147 +/- 88 mm(3); Halothane = 171 /- 91 mm(3); p = 0.477) infarct volumes were not significantly different be tween 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 st udies is consistent with influences on intraischemic pathophysiology only.