PREVENTION OF ISCHEMIA-INDUCED CEREBRAL HYPOTHERMIA BY CONTROLLING THE ENVIRONMENTAL-TEMPERATURE

Regulation of brain temperature during and after cerebral ischemia plays an important role in the evolution of neuronal damage. Therefore, it is essential to maintain brain temperature at 37-degrees-C during and after the ischemic insult. To get information about brain temperature during the experimental procedure, researchers in previous works have made various attempts to correlate between brain and body temperature during and after ischemia. In the present study, brain temperature was measured when ischemia was performed either at 30-degrees-C or at 20-degrees-C environmental temperature. For this purpose a stainless-steel guide of a temperature probe was introduced through the bregma and implanted between both hemispheres of the rat. Rats were then subjected to a 10-min period of forebrain ischemia. Cerebral temperature was measured during ischemia and up to 90 min; in some experiments up to 4 hr after ischemia. In another group of experiments, ischemia was performed also at either 30-degrees-C or 20-degrees-C environmental temperature, and histological assessment of the rat hippocampus was carried out. In addition, the influence of chlorpromazine as a hypothermic agent on the cerebral temperature and the neuronal loss was also tested at both of the experimental conditions. Recording the brain temperature at both of the selected environmental temperatures suggests that it is possible to preserve cerebral normothermia during and after ischemia by working at 30-degrees-C environmental temperature. On the other hand, brain temperature dropped sharply immediately after ischemia when working under 20-degrees-C environmental temperature, and brain tissue was thereby protected against ischemia. Moreover, the hypothermic effect of chlorpromazine was abolished at 30-degrees-C environmental temperature.