亚低温对新生鼠缺氧缺血脑损伤能量代谢的影响(英文)

目的：探讨亚低温治疗对缺氧缺血脑损伤 (HIBD)新生大鼠的脑组织葡萄糖、ATP及脑线粒体琥珀酸脱氢酶 (SDH)活性的影响及意义。方法：将HIBD模型鼠随机分为缺氧缺血常温恢复组 (IN)和亚低温干预组 (IH) ,同时设常温对照组 (NC)和亚低温对照组 (HC)。各组动物在缺氧缺血结束后不同时间点 (0 ,2 ,6 ,2 4 ,4 8,72h)断头取脑 ,测定脑匀浆葡萄糖含量、ATP含量及脑线粒体琥珀酸脱氢酶 (SDH)活性。结果：脑糖在缺氧缺血0h明显低于对照组 ,缺氧缺血 2h后即恢复正常。IN组脑ATP含量及SDH活性先行下降 ,以后逐渐恢复 ,72h达高峰 ;IH组从缺氧缺血 6h后或 2h起ATP及SDH活性均显著高于同一时间点IN组。ATP含量与SDH活性呈显著正相关 (r =0 .5 15 ,P <0 .0 1)。结论：亚低温可减轻HIBD鼠线粒体SDH活性下降 ,改善能量代谢 ,增加脑ATP合成 ,从而保护脑组织。

Effects of Moderate Hypothermia on Cerebral Energy Metabolism in Neonatal Rats with Hypoxic Ischemic Brain Damage

Objective To study the effects of moderate hypothermia on cerebral glucose and ATP contents and mitochondrial succinate dehydrogenase (SDH) activity in neonatal rats with hypoxic ischimic brain damage (HIBD). Methods Seven day old Sprague Dawley rat pups were subjected to ligation of the left carotid artery followed by exposure to hypoxia environment of 8% O 2 for 2 h, then they were randomly assigned into normothermic recovered group (IN group) and moderate hypothermic recovered group (IH group). The sham operated rats which were used as the control were assigned into the normothermic control group (NC group) and moderate hypothermic control group (HC group). The contents of glucose and ATP and activity of mitochondrial SDH were assayed at 0, 2, 6, 24, 48, 72 h after HIBD. Results The cerebal glucose contents in the IN and IH groups were significantly lower than those of the NC and HC groups 0 h after HIBD. Two hours after HIBD, the glucose content recovered to normal level. The concentration of ATP and activity of SDH in the IN group decreased first, then they recovered gradually and reached a peak 72 hours after HIBD. After 6 hours or 2 hours of HIBD, the ATP content or SDH activity of the brain in the IH group were significantly higher than those in the IN group. The ATP concentration was closely related to the SDH activity (r= 0.515 , P< 0.01 ). Conclusions Moderate hypothermia might protect brain tissue by inhibiting the decrease of SDH activity and increasing the synthesis of ATP