虚血性細胞機能障害における軽度低温の抑制作用
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概要
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It has been well known that intracellular increase in Ca^<++> induced by massive release of excitatory amino acid and by increased phospholipid metabolism during and after ischemia that plays an important role in brain damage. Furthermore, recent studies revealed that mild hypothermia (only 2-5℃ reduction of brain temperature below normothermia) provided protective effect, though the mechanism of this effect is still unclear. The present study was designed to gain further insight into the mechanism for neuroprotective effect of mild hypothermia especially focussing on the changes of intracellular signal transduction system in a model of progressive forebrain ischemia in the rats. Two series of study were performed in male Wistar rats in which the brain temperature was kept either at normothermia (37℃) or at a mild hypothermia (33℃) during the ischemic period. Forebrain ischemia (10 and 30 min duration) was producted by bilateral occlusion of the carotid artery combined with hemorrhagic hypotension (mean BP=50mmHg). In the first series of experiment, neuropathological damages were assessed by the immunohisto-chemical reactivity for microtubule-associated protein (MAP2) in the cerebral cortex, striatum, hippocampus, and thalamus. In the second series, the changes in binding for ^3H-PDBu were measured to evaluate the functional changes of protein kinase C. The progressive decrease in MAP2 immunoreactivity was observed, the order of severity being striatum>hippocampus>cerebral cortex>thalamus. The binding for ^3H-PDBu decreased by 33%, 25% in the hippocampus, cerebral cortex after 30 min of ischemia, respectively. In the mild hypothermia group, the decrease in MAP2 immunoreactivity was attenuated in the striatum and hippocampus after 30 min of ischemia. This decrease in ^3H-PDBu binding was significantly less in hippocampus. These results suggest that, in progressive ischemia, mild hypothermia may ameliorate the cytoskeletal damages possibly by inhibiting the perturbation of intracellular signal transduction system.
- 九州歯科学会の論文
- 2004-06-25