Barbiturate-induced coma therapy for focal cerebral ischemia

Abstract

The therapeutic effect of barbiturate coma following middle cerebral artery (MCA) occlusion was studied in primates [Papio anubis]. The relationship of the efficacy of barbiturate protection to the presence or absence of recirculation was examined. Pentobarbital therapy was begun 30 min after MCA occlusion. Barbiturate-induced coma, with its attendant monitoring, was safely tolerated by primates for 96 h. Six h of MCA occlusion followed by recirculation resulted in a neurological deficit that was worse than the neurological deficit produced by permanent MCA occlusion. Barbiturate-induced coma for 96 h, initiated 30 min after the onset of MCA occlusion, in the absence of reperfusion, was detrimental. Barbiturate-induced coma for 96 h, initiated 30 min after MCA occlusion, with the establishment of reperfusion at 6 h, provided nearly complete protection from ischemic damage.