腺苷A1受体拮抗剂对L-NAME预处理第二窗心肌保护作用的影响

Effects of Adenosine A1 Receptor Antagonist on L-NAME-induced the Second Window Myocardial Protection in Isolated Rat Hearts

目的探讨药物L-NAME预处理后第二窗心肌保护作用是否与腺苷A1受体激活有关。方法将30只SD大鼠随机分成3组,每组10只,即缺血对照组、L-NAME预处理组及拮抗剂组,每组均于给药后24h建立离体大鼠心脏Langendorff灌注模型,全心缺血60min,再灌注120min,于S15、R1、R60、R1204个时间点观察HR、LVDP、CF的变化,检测冠脉流出液中cTnI的变化,电镜观察缺血后心肌的超微结构改变。结果全组心率缺血前无差别,拮抗剂组缺血后心率较L-NAME组慢,两者差异有统计学意义(P<0.05),与缺血对照组无差别;拮抗剂组的LVDP较L-NAME预处理组低,两者差异有统计学意义(P<0.05),与缺血对照组无差别;拮抗剂组的CF较L-NAME预处理组少,两者差异有统计学意义(P<0.05),与缺血对照组无差别;拮抗剂组的cTnI较L-NAME预处理组显著增高(P<0.05),与缺血对照组无差别;电镜下拮抗剂组及缺血对照组心肌超微结构的损伤程度较L-NAME预处理组重。结论腺苷A1受体拮抗剂DPCPX阻断了L-NAME预处理第二窗的心肌保护作用,腺苷A1受体可能是L-NAME预处理引起心肌保护作用的启动因子。

Objective To determine whether L-NAME-induced the second window myocardial protection is activated by adenosine receptor A1. Methods Three groups of Sprague-Dawley rats （control, n=10; L-NAME, n= 10;DPCPX,n=10） were studied in an isolated buffer-perfused heart model. The hearts were subjected to 60 minutes global ischemia and 120 minutes of reperfusion.Heart rate,left ventricular developed pressure,coronary flow and cardiac troponin I were recorded and analyzed. The injury of cardiac tissue was evaluated under the electron microscopy. Results During reperfusion, heart rate was slower in the DPCPX group than that in the L-NAME group.The coronary flow as well as the left ventricular developed pressure were lower in the DPCPX group than that in the L-NAME group before ischemia and remained so until the end of the experimentation.Cardiac troponin I release was higher in the DPCPX group than that in L-NAME group during experimentation.The injury of myocardial cell in the DPCPX was more serious than in the L-NAME pre-treated group.Conclusion Adenosine A1 receptors are involved in L- NAME-induced myocardial the second window of protection.Adenosine A1 receptors may be a trigger of L-NAME- induced myocardial the second window of protection.