NEURONAL DAMAGE, GLIAL RESPONSE AND CEREBRAL METABOLISM AFTER HYPOTHERMIC FOREBRAIN ISCHEMIA IN THE RAT

We investigated the effect of 30-degrees-C whole body hypothermia on neuronal injury, astroglial reactivity and intracellular pH in rats subjected to 15 min of forebrain ischemia. Experimental groups included: (1) normothermic ischemia (n = 8), ischemia induced under 37-degrees-C body temperature, (2) hypothermic ischemia (n = 6), ischemia induced under 30-degrees-C body temperature. Cerebral intracellular pH was measured using in vivo P-31 NMR spectroscopy over 7 days. Neuronal injury and astrocytic reactivity were evaluated using hematoxylin and eosin staining, and immunoreactivity to glial fibrillary acidic protein, respectively. Normothermic animals revealed significant alkalosis (P < 0.01) at 48 h after ischemia compared to the pre-ischemic value. No significant intracellular pH change was detected after ischemia in the hypothermic group. Ischemic neuronal injury was prevented in the hypothermic animals. compared to the severe neuronal injury found in the normothermic animals (P < 0. 0 1) . The marked astrocytosis of normothermic animals was significantly inhibited in the hypothermic animals (P < 0.01). Our data indicate, that hypothermia significantly inhibits neuronal injury as well as post-ischemic alkalois and astrocytosis, induced by 15 min of forebrain ischemia in the rat.