CARDIAC ARREST-INDUCED GLOBAL CEREBRAL-ISCHEMIA STUDIED IN-VITRO

The goal of the present study was to characterize the effects of chest compression-induced global cerebral ischemia on the hippocampal slice preparation. One of the characteristics of rats exposed to such cardi ac arrest is a high susceptibility to sound-induced seizures. We teste d audiogenic seizures as an in vivo indicator of ischemic cerebral dam age and as a possible small animal model of epilepsy. The results of t hese tests were reported eleswhere. Long-Evans male rats (200-350 g) w ere subjected to 7 min of chest compression sufficient to stop the pum ping action of the heart. The rats were then revived using cardiopulmo nary resuscitation. Evaluation of cerebral damage following cardiac ar rest and resuscitation was performed in vitro, by testing neuronal res ponses to electrical stimulation in hippocampal slices prepared from t hese animals. Sham control animals were used for comparisons. Twenty-o ne to 146 days after rats were chest-compressed, hippocampal slices we re prepared. Sham control rats, anesthetized but not chest-compressed, were sacrificed one week later for preparation of slices. Rats in a s econd group exposed to 7-min chest compression, were sacrificed at dif ferent time intervals after their resuscitation (from 1 h to 7 days); hippocampal slices were prepared for electrophysiological analysis of neuronal damage. The results of these studies indicate that 3 weeks or longer after chest compression the evoked CA1 population spike amplit ude in hippocampal slices was significantly attenuated; in 60% of thes e slices an epileptiform response was evoked. An increased proportion of slices prepared from rats 1 to 48 h after chest compression showed an augmentation in the amplitude of the evoked population spike; 72 h and up to 7 days after chest compression, an attenuation in the evoked CA1 population spike amplitude was observed, signaling delayed neuron al damage.