HYPOTHYROIDISM PROTECTS THE BRAIN DURING TRANSIENT FOREBRAIN ISCHEMIAIN GERBILS

The mechanisms by which brain cells die after brief episodes of cerebr al ischemia are not fully understood. In certain brain regions this da mage may not be apparent for days. Hypothyroidism is known to decrease cerebral metabolism. We postulated that this slowing in cerebral meta bolism may be neuroprotective after transient cerebral ischemia. To te st this hypothesis, a total of 10 gerbils had thyroidectomies performe d 2 weeks prior to ischemia. Six gerbils served as euthyroid controls. All animals were exposed to 5 min of transient ischemia and sacrifice d 7 days after the insult. Silver degeneration staining was used for h istological evaluation. Hippocampal damage [subiculum (P < 0.001), CA1 (P = 0. < .001), CA3 (P < 0.05), and CA4 (P < 0.001)] was significant ly less in the hypothyroid animals. There was also significantly less damage in the cerebral cortex (P < 0.05) and thalamus (P < 0.05) in th e hypothyroid animals. The exact mechanism of this protection is not f ully understood but could be secondary to a decrease in the metabolic activity, or a reduced generation of free radicals (as is seen with pr otection from ischemia in kidney and liver under hypothyroid condition s). Further studies are required in order to gain a better understandi ng of the protective effects of hypothyroidism on cerebral ischemia. ( C) 1994 Academic Press, Inc.