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Neuroprotection of mild hypothermia beginning at different time intervals on cerebral ischemia/reperfusion injury
Author(s) -
Zhang H.,
Tong E. T.
Publication year - 2002
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.81.s1.42_2.x
Subject(s) - hypothermia , ischemia , anesthesia , medicine , lipid peroxidation , neuroprotection , brain ischemia , glutathione , cerebral edema , chemistry , oxidative stress , biochemistry , enzyme
The effects of mild hypothermia beginning at different time intervals on cerebral ischemia was studied in SD rats which were divided into sham‐operated, normothermia (37–38°C) ischemia and mild hypothermia (31–32°C) group. The latter was subdivided into: 240 min hypothermia, 30 min normothermia plus 210 min hypothermia, 60 min normothermia plus 180 min hypothermia and 90 min normothermia plus 150 min hypothermia. Global cerebral ischemia was induced by modified 4‐vessel occlusion model. 240 min reperfusion following 20 min cerebral ischemia. Results showed that in normothermia group, the amount of SOD, GSH‐Px, GSH, ATP, K + were lower and MDA, lactate, water content, Ca ++ were higher than those in sham‐operated group. Mild hypothermia beginning immediately within 60 min delayed the consumption of SOD, GSH‐Px, GSH, ATP and decreased the accumulation of MDA, lactate, water content and Ca ++ as compared with normothermia group. Mild hypothermia beginning immediately within 30 min significantly decreased the elevation of Na + , Ca ++ and increased K + in brain tissue when compared with normothermia. Mild hypothermia beginning immediately at 90 min has little effect on the content of SOD, GSH‐Px, GSH, MDA, lactate, ATP, water content and Na + , K + , Ca ++ as compared with the normothermia group. Mild brain hypothermia beginning immediately after ischemia delay consumption of endogenous antioxidant enzyme and energy metabolism, decrease accumulation of lactate and lipid peroxidation and the development of brain edema, which is involved in the mechanism of cerebral protection by mild hypothermia. Mild hypothermia limits ischemia injury beginning immediately within 30 or 60 min, but lost its function when beginning at 90 min following ischemia.