亚低温对急性心肌梗死SD大鼠心肌保护的实验研究

Experimental study on mild hypothermia on myocardial protection in SD rats with acute myocardial infarction

目的实验观察诱导亚低温(32℃~36℃)治疗对SD大鼠急性心肌梗死后心肌的保护。方法40只健康SD大鼠随机分为两组,即常温对照组和诱导亚低温实验组,建立急性心肌梗死(AMI)实验模型,结扎左前降支近端,结扎后1 h后再解除结扎,4 h后分别测定两组大鼠的左心室射血分数(LVEF)、心率(HR)和左室舒张末期压(LVEDP)、心肌组织中超氧化物歧化酶(SOD)和丙二醛(MDA)水平及TUNEL法检测心肌细胞凋亡率。结果亚低温组治疗后LVEF、SOD水平明显高于常温组,差异有统计学意义(P<0.05);亚低温组治疗后HR、LVEDP、MDA水平、心肌细胞凋亡率均明显低于常温组,差异有统计学意义(P<0.05)。结论亚低温治疗通过降低心室率,提高左心室射血分数,改善左室舒张末期压以及降低心肌的氧化应激损伤及细胞凋亡率,来保护左心室心功能,从而达到对急性心肌梗死的缺血/再灌注心肌的保护,最终降低病死率。

Objective To observe the myocardial protection of induced mild hypothermia(32℃~36℃)in SD rats with acute myocardial infarction through experiment.Methods A total of 40 healthy SD rats were randomly divided into two groups as the normal temperature control group and the induced mild hypothermia experimental group.An acute myocardial infarction(AMI)experimental model was established.The proximal left anterior descending artery was ligated and then released 1 hour after ligation.After 4 hours,the left ventricular ejection fraction(LVEF),heart rate(HR),left ventricular end diastolic pressure(LVEDP),superoxide dismutase(SOD)level,and malondialdehyde(MDA)level were detected in the two groups.TUNEL method was used to detect myocardial cell apoptosis rate.Results After treatment,the levels of LVEF and SOD in the mild hypothermia group were significantly higher than those in the normal temperature group,with statistically significant differences(P<0.05).After treatment,the levels of HR,LVEDP,MDA,and the myocardial cell apoptosis rate in the mild hypothermia group were significantly lower than those in the normal temperature group,with statistically significant differences(P<0.05).Conclusion Mild hypothermia therapy protects left ventricular function by decreasing HR,increasing LVEF,improving LVEDP,and reducing myocardial oxidative stress damage and cell apoptosis rate,to protect ischemia/reperfusion myocardium after acute myocardial infarction,to ultimately reduce mortality rate.