Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2007
[Effect of cerebral mild hypothermia on cerebral mitochondrial ATPase activity in neonatal rats with hypoxic-ischemic brain damage].
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Yao Li, Cheng Lin, Yu Li-Jun
Аннотация
OBJECTIVE: To study the effect of cerebral mild hypothermia on cerebral mitochondrial ATPase activities in neonatal rats with hypoxic-ischemic brain damage (HIBD).
METHODS: Eighty-four seven-day-old Wistar rats were randomly assigned into four groups: sham-operated normothermic, sham-operated mild hypothermic, HIBD normothermic and HIBD mild hypothemic. HIBD was induced by left common carotid artery ligation, followed by 8% hypoxia exposure. At each time interval of 2, 6, and 12 hrs post-hypoxia-ischemia (HI), 7 rats were sacrificed and the brain tissues were sampled for detecting the activities of mitochondrial Na+K+ATPase and Ca2+ATPase.
RESULTS: The activities of mitochondrial Ca2+ATPase decreased significantly in the two HIBD groups compared with those of the two sham-operated groups at 2, 6, and 12 hrs post-HI. The HIBD mild hypothemic group had higher mitochondrial Ca2+ATPase activities compared with the HIBD normothermic group at 2, 6, and 12 hrs post-HI (5.25 +/- 0.61 micromol/mgPr.h vs 3.17 +/- 0.81 micromol/mgPr.h 4.59 +/- 0.81 micromol/mgPr.h vs 2.26 +/- 0.53 micromol/mgPr.h4.61 +/- 0.62 micromol/mgPr.h vs 1.31 +/- 0.78 micromol/mgPr.H, respectively) (P < 0.01). The activities of mitochondrial Na+K+ATPase decreased significantly in the two HIBD groups compared with those of the two sham-operated groups at 6 and 12 hrs post-HI. A significant difference was observed in the mitochondrial Na+K+ATPase activities between the HIBD mild hypothemic and HIBD normothermic groups at 6 and 12 hrs post-HI (5.25 +/- 0.66 micromol/mg Pr.h vs 3.76 +/- 0.78 micromol/mgPr.h, 4.74 +/- 0.80 micromol/mgPr.h vs 3.12 +/- 0.53 micromol/mgPr.h; P < 0.01).
CONCLUSIONS: Mild hypothermia following HIBD inhibits the decline in cerebral mitochondrial Ca2+ and Na+K+ ATPase activities in neonatal rats, thus providing protective effects against HIBD.
METHODS: Eighty-four seven-day-old Wistar rats were randomly assigned into four groups: sham-operated normothermic, sham-operated mild hypothermic, HIBD normothermic and HIBD mild hypothemic. HIBD was induced by left common carotid artery ligation, followed by 8% hypoxia exposure. At each time interval of 2, 6, and 12 hrs post-hypoxia-ischemia (HI), 7 rats were sacrificed and the brain tissues were sampled for detecting the activities of mitochondrial Na+K+ATPase and Ca2+ATPase.
RESULTS: The activities of mitochondrial Ca2+ATPase decreased significantly in the two HIBD groups compared with those of the two sham-operated groups at 2, 6, and 12 hrs post-HI. The HIBD mild hypothemic group had higher mitochondrial Ca2+ATPase activities compared with the HIBD normothermic group at 2, 6, and 12 hrs post-HI (5.25 +/- 0.61 micromol/mgPr.h vs 3.17 +/- 0.81 micromol/mgPr.h 4.59 +/- 0.81 micromol/mgPr.h vs 2.26 +/- 0.53 micromol/mgPr.h4.61 +/- 0.62 micromol/mgPr.h vs 1.31 +/- 0.78 micromol/mgPr.H, respectively) (P < 0.01). The activities of mitochondrial Na+K+ATPase decreased significantly in the two HIBD groups compared with those of the two sham-operated groups at 6 and 12 hrs post-HI. A significant difference was observed in the mitochondrial Na+K+ATPase activities between the HIBD mild hypothemic and HIBD normothermic groups at 6 and 12 hrs post-HI (5.25 +/- 0.66 micromol/mg Pr.h vs 3.76 +/- 0.78 micromol/mgPr.h, 4.74 +/- 0.80 micromol/mgPr.h vs 3.12 +/- 0.53 micromol/mgPr.h; P < 0.01).
CONCLUSIONS: Mild hypothermia following HIBD inhibits the decline in cerebral mitochondrial Ca2+ and Na+K+ ATPase activities in neonatal rats, thus providing protective effects against HIBD.