2004•Journal of Apoplexy and Nervous DiseasesRequires access

The effect of local mild hypothermia on the infarct volume and the glial fibrillary acidic protein change after focal cerebral ischemia and reperfusion in rats

Yuhua Zhang

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Abstract

Objective To observe the effect of local intraischemic and postischemic mild hypothermia on cerebral infarction and the expression of glial fibrillary acidic protein (GFAP) after focal cerebral ischemia and reperfusion injury. Methods Reversible middle cerebral artery occlusion was performed with modified Koizumi’s model. The brain temperature was lowered to 32 ℃~33℃ in focal cerebral ischemia rodent models by feedback regulated semiconductor cooling therapy,started at 30 minutes after the ischemic onset and maintained throughout the period of ischemia and reperfusion. The GFAP expression was investigated with immunohistochemistry,the infarct volume was examined with 2,3,5-triphenyl-tetrazolium chloride staining. Results A significant reduction(P 0.05) in infarct volume was found in the hypothermia group compared with the normothermia group. Compared with the normothermia group,hypothermic treatment also inhibited the overexpression of GFAP. Conclusion Intraischemic and postischemic mild hypothermia could markedly inhibit the activation and swelling of astrocyte as well as reduce ischemic brain damage in a focal model of transient cerebral ischemia in rats.

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Objective To observe the effect of local intraischemic and postischemic mild hypothermia on cerebral infarction and the expression of glial fibrillary acidic protein (GFAP) after focal cerebral ischemia and reperfusion injury. Methods Reversible middle cerebral artery occlusion was performed with modified Koizumi’s model. The brain temperature was lowered to 32 ℃~33℃ in focal cerebral ischemia rodent models by feedback regulated semiconductor cooling therapy,started at 30 minutes after the ischemic onset and maintained throughout the period of ischemia and reperfusion. The GFAP expression was investigated with immunohistochemistry,the infarct volume was examined with 2,3,5-triphenyl-tetrazolium chloride staining. Results A significant reduction(P 0.05) in infarct volume was found in the hypothermia group compared with the normothermia group. Compared with the normothermia group,hypothermic treatment also inhibited the overexpression of GFAP. Conclusion Intraischemic and postischemic mild hypothermia could markedly inhibit the activation and swelling of astrocyte as well as reduce ischemic brain damage in a focal model of transient cerebral ischemia in rats.

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Available abstract

Objective To observe the effect of local intraischemic and postischemic mild hypothermia on cerebral infarction and the expression of glial fibrillary acidic protein (GFAP) after focal cerebral ischemia and reperfusion injury. Methods Reversible middle cerebral artery occlusion was performed with modified Koizumi’s model. The brain temperature was lowered to 32 ℃~33℃ in focal cerebral ischemia rodent models by feedback regulated semiconductor cooling therapy,started at 30 minutes after the ischemic onset and maintained throughout the period of ischemia and reperfusion. The GFAP expression was investigated with immunohistochemistry,the infarct volume was examined with 2,3,5-triphenyl-tetrazolium chloride staining. Results A significant reduction(P 0.05) in infarct volume was found in the hypothermia group compared with the normothermia group. Compared with the normothermia group,hypothermic treatment also inhibited the overexpression of GFAP. Conclusion Intraischemic and postischemic mild hypothermia could markedly inhibit the activation and swelling of astrocyte as well as reduce ischemic brain damage in a focal model of transient cerebral ischemia in rats.

Key concepts: Glial fibrillary acidic protein, Ischemia, Medicine, Hypothermia, Anesthesia, Cerebral infarction, Astrocyte, Infarction

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