目的：研究头部贴敷式亚低温治疗对缺氧缺血脑损伤（hypoxic-ischemic brain damage, HIBD）新生大鼠的脑组织线粒体ATP酶活性的影响，以进一步探讨亚低温对缺氧缺血脑组织的保护机制。方法：将84只Wistar新生鼠随机分为4组：假手术常温对照组、假手术亚低温对照组、HIBD模型常温恢复组、HIBD模型亚低温治疗组。各组动物在HI后不同时间点（2，6，12 h）断头取脑，提取脑组织线粒体并测定其中Na+K+ATP酶和Ca2+ATP酶活性。结果①HIBD常温恢复组及亚低温治疗组在2，6，12 h时Ca2+ATP酶活性均呈下降趋势，分别为3.17±0.81，2.26±0.53，1.31±0.78 μmol/mgPr．h及5.25±0.61，4.59±0.81，4.61±0.62 μmol/mgPr．h，但亚低温治疗各组该酶活性均明显高于相应的常温组（P<0.01）。②HIBD常温及亚低温2 h组Na+K+ATP酶活性较之假手术组无明显改变，6 h、12 h组该酶活性明显低于假手术组，分别为3.76±0.78，3.12±0.53 μmol/mgPr．h及5.25±0.66、 4.74±0.80 μmol/mg Pr．h，但亚低温治疗组明显高于相应常温组（P<0.01）。结论 贴敷式局部亚低温可增加HIBD后脑线粒体ATP酶活性，保护脑组织。［中国当代儿科杂志，2007，9（4）：305-307］

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 μmol/mgPr. h vs 3.17±0.81 μmol/mgPr, h, 4.59±0.81 μmol/mgPr. h vs 2.26±0.53 μmol/mgPr. h, 4.61±0.62 μmol/mgPr. h vs 1.31±0.78 μmol/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 μmol/mg Pr. h vs 3.76±0.78 μmol/mgPr. h, 4.74±0.80 μmol/mgPr. h vs 3.12±0.53 μmol/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.［Chin J Contemp Pediatr, 2007, 9 (4):305-307］