POSTISCHEMIC HYPOTHERMIA FAILS TO REDUCE ISCHEMIC-INJURY IN GERBIL HIPPOCAMPUS

The objective of this study was to determine whether postischemic hypothermia diminishes ischemic injury in gerbil hippocampus. Cerebral ischemia was produced by occluding both carotid arteries for 5 min, while maintaining the temperature of the cranium and rectum at 38-degrees-C. Upon recirculation, the animals were divided into three groups: normothermic (38-degrees-C), moderately hypothermic (33-degrees-C), and deeply hypothermic (23-degrees-C). In the normothermic group, cranial and rectal temperatures were maintained at 38-degrees-C for 30 min and 2 h, respectively, prior to the removal of the temperature probes. In the moderately hypothermic group, cranial and rectal temperatures were reduced within 10 min to 33-degrees-C for 1 h, and then rewarmed to 38-degrees-C. In the deeply hypothermic group, rectal temperature was lowered within 10 min to 23-degrees-C for 2 h prior to rewarming to 38-degrees-C. After recovery for 1 week, the extent of histologic injury in the hippocampus was assessed in stained sections. Maximal injury was present in the CA1 subfield in all three groups. These results indicate that hippocampal injury was not diminished by postischemic hypothermia during the first 2 h of reperfusion. Thus, pharmacologic studies of postischemic protection in the gerbil model may not be strongly influenced by transient postischemic hypothermia.