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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。
Objective To investigate the effects of mild hypothermia on glucose, ATP and brain mitochondrial succinate dehydrogenase (SDH) activity in neonatal rats with hypoxic-ischemic brain damage (HIBD). Methods HIBD model rats were randomly divided into two groups: hypoxic-ischemic hypothermia recovery group (IN) and mild hypothermia intervention group (IH), and normal control group (NC) and mild hypothermia control group (HC). The brain of each group was decapitated at different time points (0, 2, 6, 24, 48, 72h) after hypoxia-ischemia. The contents of glucose, ATP and brain mitochondrial succinate dehydrogenase (SDH) activity. Results Brain glucose in hypoxia-ischemia 0h significantly lower than the control group, 2h after hypoxia-ischemia returned to normal. ATP content and SDH activity in IN group decreased first, then gradually recovered and reached the peak at 72h. The activity of ATP and SDH in IH group was significantly higher than that in IN group at 6h or 2h after hypoxic-ischemia. There was a significant positive correlation between ATP content and SDH activity (r = 0.515, P <0.01). Conclusion Mild hypothermia can reduce mitochondrial SDH activity in HIBD rats, improve energy metabolism and increase brain ATP synthesis, thus protecting brain tissue.