Pentobarbital protection from cerebral infarction without suppression of edema.

Abstract

We studied the mechanism of barbiturate protection from focal cerebral infarction in cats by examining in detail edema formation 72 hours after acute, permanent occlusion of the left middle cerebral artery (LMCA). Neurological function, gas exchange, vital signs, and intracranial pressure (ICP) were observed during the post-occlusion period, and infarct size and cerebral edema were measured after sacrifice. Infarct size was reduced only when pentobarbital was given before occlusion and continued for 24 hours. Edema formation was not suppressed even though the extent of infarction was. Clinical evidence of stroke developed and ICP rose in most cats after occlusion despite the presence of pentobarbital sufficient to reduce infarct size. Elevated ICP accounted for most premature deaths despite intensive cardiopulmonary support. Water and electrolyte changes in the ischemic hemisphere continued to develop throughout the 72 hour post-occlusion period in pentobarbital-treated cats, suggesting that resolution of edema was delayed by the drug. We conclude that pentobarbital reduces infarct size and attenuates the expected time course of ischemic edema in cats, but that the drug has little effect on the severity of edema that develops after arterial occlusion.