Abstract
A possible cerebroprotective effect of halothane was investigated in a canine model of 5-min global cerebral ischemia. In pentobarbital-anesthetized dogs, additional inhalation of 0.5 to 1% halothane prior to ischemia prevented the post-ischemic dysfunction of the vagal component of reflex bradycardia. In contrast, pretreatment with thiopental at 10 mg/kg, i.v. failed to prevent it. The influence of ischemia in the absence of anesthetics was similar to that under barbiturate anesthesia. The results suggest that halothane, but not barbiturate, may actively protect the vagal baroreflex system from ischemia.
