在小鼠心跳骤停期间应用中度低温对复苏后抗氧化物酶活性的影响

目的：低温在许多小鼠心跳骤停后复苏模型的研究中被证实是有效的。心跳骤停后释放的氧自由基是产生继发性损伤的一个重要机制。本研究旨在探索心跳骤停期间应用中度低温对复苏后抗氧化物酶活性的影响。方法：用氯化钾诱导8min心跳骤停。此实验分为常温心跳骤停组（NCA）、低温心跳骤停组（HCA）TL对照组。HCA组在心跳骤停5min后开始降温使核心温度维持在（30．0±1．0）℃。应用胸部按压和肾上腺素来复苏。在心跳骤停两组各选择三个时间点：复苏后1h、4h和24h。测量超氧化物歧化酶（SOD）和过氧化氢酶（CAT）在心脏和肝脏的活性。结果：实验动物在HCA组比常NCA组生存率高。HCA组比NCA组复苏时间明显延长。与NCA组相比，HCA组复苏后24h的SOD活性在肝脏表达明显降低。与NCA组相比，HCA组复苏后4h的CAT活性在肝脏表达显著增高。结论：在心跳骤停过程中，与正常体温相比，应用中度低温能够提高生存率。与正常体温相比较，在心跳骤停中期间应用中度低温不影响心脏的SOD与CAT活性，应用中度低温在肝脏可延迟性抑制SOD的活性并且短暂提高CAT活性。

Antioxidant Enzymes Activity Analysis when Inducing Moderate Hypothermia during Cardiac Arrest of Mice

Objective： Hypothermia has been approved efficacy in mouse cardiac arrest model in series reports. The release of toxic reactive oxygen species is an important secondary injury mechanism after cardiac arrest. This study was to explore the influence on antioxidant enzymes when intra-arrest cooling was induced during cardiac arrest. Methods： Eight minutes cardiac arrest was induced by potassium chloride. Sham, normothermia cardiac arrest （NCA） and hypothermia cardiac arrest （HCA） groups were studied in this experiment. Intra-arrest cooling was performed after 5 min cardiac arrest to get target temperature （30.0＋ 1.0） ~C in the HCA groups. Resuscitation was performed by chest compression and epinephrine. Three time points were chosen in the NCA and the HCA groups： resuscitation time （RT） 1 h, 4 h and 24 h. Superoxide dismutase （SOD） and catalase （CAT） activity were measured in heart and liver. Results： The survival in the HCA groups is higher than in the NCA groups. Resuscitation time is significantly longer in the HCA groups than the NCA groups. The HCA group showed significantly decrease SOD activity in liver compared with the NCA group at RT 24 h. CAT activity in the liver increased at RT 4 h in the HCA group compared to the NCA group. Conclusions： Intra-arrest cooling to moderate hypothermia improved survival compared to normothermia cardiac arrest but incidental to heart autorhythmicity inhibition. SOD and CAT activity in heart were not influenced by hypothermia used during cardiac arrest. SOD activity was delayed inhibited by moderate hypothermia and CAT activity was temporarily increased when intra arrest cooling was induced compared to the NCA group in liver.