Resuscitation of the rabbit brain after acute complete ischemia lasting up to one hour: pathophysiological and pathomorphological observations.

This study was conducted to investigate the degree of insult from arrest of cerebral blood flow leading to total brain ischemia, as a model for brain resuscitation studies in rabbits. In normothermic rabbits under light barbiturate anesthesia, cerebral blood flow was completely arrested for 5, 10, 15, 20, 30, 45 and 60 min by intrathoracic occlusion of the brachiocephalic trunk, the left subclavian and both internal thoracic arteries. Arterial blood pressure, arterial pH, arterial blood gases, cerebral blood flow, intracranial pressure, hematocrit and end tidal CO2 were monitored and recorded before, during and for 8 h after reperfusion. Disappearance and return of spontaneous EEG activity, vasomotor and respiratory centers were also recorded. During ischemia, the EEG was suppressed within 15 s and vasomotor and respiratory centers within 3-6 min. In all animals with 5, 10, 15 and 20 min cerebral ischemia bioelectric activity of brain cortex, vasomotor and respiratory centers returned upon recirculation. In about 50% animals with 30, 45 and 60 min ischemia recovery of basic brain function did not occur. After different periods of ischemia, histopathologic lesions were located mostly in the frontal cortex and hippocampus with ischemic neuronal change as the most frequent structural change. Brain cell necrosis was seen after successful resuscitation. This study indicates the feasibility of an ischemic insult in rabbits for use in resuscitation studies.