U83836E对大鼠离体心肌缺血再灌注损伤的保护作用

Protective Effect of U83836E on Ischemia-Reperfusion Injury in Isolated Rat Heart

目的探讨第2代拉扎碱(U83836E)对大鼠离体心肌缺血再灌注损伤的保护作用。方法用Langendofff灌注系统,建立大鼠离体全心缺血再灌注损伤模型。观察不同时间注射U83836E对复灌后心脏舒缩功能、心肌乳酸脱氢酶(LDH)、肌钙蛋白(cTnT)及热休克蛋白70(HSP70)的影响。结果 U83836E可改善大鼠离体心脏缺血再灌注后的功能,与模型组比较,左心室收缩压(LVSP)升高(P<0.01),左心室舒张末压(LVEDP)降低(P<0.05),左心室压力最大上升和下降速率(±dp/dtmax)加快(P<0.01);冠脉流出液中的乳酸脱氢酶和肌钙蛋白含量减少(P<0.01),并可诱导心肌组织产生热休克蛋白70(P<0.01)。结论 U83836E对大鼠离体心肌缺血再灌注损伤具有保护作用。

OBJECTIVE To study the protective effect of U83836E （lazaroids） on ischemia-reperfusion injury （IRI） in isolated rat heart. METHODS The isolated rat heart models of IRI were developed by linking the isolated rat heart to Langendorff perfusionsystem. U83836E was injected in different time, the rat heart function of ischemia-reperfusion was observed. Lactate dehydrogenase （LDH） and the cardiae treponin（cTnT） content in the outflow of coronary artery, and heat shock protein70 （HSP70） of myocardial tissue were measured. RESULTS Compared with model group of ischemia-reperfusion, in the presence of U83836E,left ventricuIar systolic pressure （ LVSP）, the maximum rise rate of left ventricular pressure （ ＋ dp/dtmax ） were increased （ P 〈 0. 01 ） ,left ventrieular enddiastolic pressure（LVEDP） was depressed（P 〈 0. 05 ） , the maximum fall rate left of ventricular pressure （ - dp/dtmax ） was accelerated （P 〈0. 01 ）. The content of LDH and cTnT in effluent samples of U83836E group（A group or B group） were lower than that in modelgroup（P 〈0. 01 ） ,the expression of HSP70 in myocardial tissue was increased（P 〈0. 01 ）. CONCLUSION U83836E has protective effect on myocardial ischemia-reperfusion injury in isolated rat heart .