左旋卡尼汀对兔在心肌缺血/再灌注损伤状态下抗氧化指标分析  

Antioxidant index of L-carnitine in rabbits with ischemia-reperfusion injury in vivo

作　　者：夏经钢[1] 王丽娟[1] 胡健[1] 

机构地区：[1]中国医科大学附属第一医院循环内科,辽宁沈阳110001

出　　处：《中国医科大学学报》2006年第4期364-366,共3页Journal of China Medical University

摘　　要：目的:探讨左旋卡尼汀在心肌缺血/再灌注损伤状态下对心肌的抗氧化机制。方法:健康新西兰大白兔25只,制备兔缺血/再灌注模型,缺血30 m in,再灌注3 h。1组丝线穿过冠状动脉左室支但不结扎;2组M I后静脉滴注生理盐水至实验结束;3组M I后给予左旋卡尼汀3.0 g加入生理盐水250 m l静脉滴注至实验结束。观察指标包括:缺血/再灌注过程中心电图的动态改变;再灌注结束后动脉血游离脂肪酸(FFA)和超氧化物歧化酶(SOD)的含量及组织中Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶活性;用W estern b lot法检测结扎点以下5 mm处左心室全层心肌热休克蛋白70(HSP70)含量。结果:2组和3组均造成明显的心电图动态改变,与2组比较,3组的心电图ST段出现有效改善;3组与2组相比,FFA含量显著减少(P<0.05);Na+-K+-ATP酶,Ca2+-Mg2+-ATP酶活性及SOD、HSP70含量显著增多(P<0.05)。结论:左旋卡尼汀对心肌缺血/再灌注损伤有保护作用。这种基本保护机制可能是左旋卡尼汀诱导产生了大量的HSP70而发挥作用的。Objective： To study the effect of L-camitine on ischemia-reperfusion injury in rabbit myocardium in vivo and the possible mechanism. Methods： Myocardial ischemia-reperfusion （MIR） models were established in healthy New Zealand rabbits by performing 30-minute myocardial ischemia followed by 3-hour reperfusion. Anesthetized rabbits were randomly divided into 3 groups： group 1 （ n = 5）, in which left anterior descending coronary artery was exposed and a silk thread was placed around the artery but not tied; group 2 （ n = 10）, in which saline was injected into sublingual vein after myocardial ischemia; group 3 （ n = 10）, in which L-carnitine of 3.0 g and saline of 250 ml were intravenously injected after myocardial ischemia. The changes of echocardiogram （ECG） were recorded. The contents of free fatty acid （FFA） and superoxide dismutase （SOD） and the activities of Na^＋ -K^＋ -ATPase and Ca^2＋ -Mg^2＋- ATPase were determined after reperfusion. The content of heat shock protein-70 （HSP70） in the left ventricular myocardium that was 5 mm away from the ischemia-reperfusion region was determined by Western blot. Results. The changes of EGC were found in both group 2 and group 3. The ECG ST segment in group 3 was improved better than that in group 2. Compared with group 2, the content of FFA significantly decreased and the content of SOD and the activities of Na^＋ -K^＋ -ATPase and Ca^2＋ -Mg^2＋ -ATPase significantly increased in group 3 （ P 〈 0.05）. The content of HSP 70 in group 3 was significantly higher than that in group 2. Conclusion： L-carnitine can protect the myocardium from ischemia-reperfusion injury by inducing β-oxidation with free fatty acid, improving energy metabolism, and stabilizing cell membrane. The possible mechanism may be that L-camitine induces the production of HSP70.

关 键 词：心肌缺血/再灌注 左旋卡尼汀 热休克蛋白70 兔 

分 类 号：R542.2[医药卫生—心血管疾病]