抄録
The reversibility of neuronal suppression was evaluated in a canine model subjected to global ischemia for 5, 15, or 30 minutes via temporary occlusion of the innominate and left subclavian arteries plus hypotension induced by withdrawal of blood. Systemic blood pressure was decreased until the electroencephalograph became flat and somatosensory evoked potentials (SEP) were undetectable. Recirculation was instituted by release of the occluded arteries and replacement of systemic blood. Recovery of neuronal function following recirculation was assessed in terms of recovery of the primary SEP amplitude (V1) and the cerebral metabolic rate of oxygen (CMRO2), which was calculated by the difference in oxygen concentrations in blood from the femoral artery and the superior sagittal sinus. Also, the effects of mannitol (2 g/kg) and glycerol (1 g/kg) on recovery of neuronal activity were investigated in the 15-minute ischemia model. The agents were intravenously administered prior to production of ischemia or within 30 minutes of recirculation. SEP (V1) recovered well in the 5-minute ischemia group, but in the 15 and 30-minute groups remained at less than 52% of the control values for 6 hours following recirculation. CMRO2 exceeded the control values from 1 to 6 hours following recirculation in the 5-minute ischemia group, which suggested enhancement of metabolism, but in the 15- and 30-minute groups remained lower than in the controls for 6 hours. In animals given mannitol prior to ischemia, SEP (V1) and CMRO2 recovered well; at 4 hours after recirculation, recovery in this group was significantly better than in the other groups. Neither animals given mannitol just after recirculation nor those given glycerol before or after ischemia recovered during 4 hours of observation. The results strongly suggest that, following ischemia of 5 to 15 minutes' duration, brain electrical activity may recover completely and that administration of mannitol prior to the production of ischemia enhances neuronal recovery.
