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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 investigate whether myocardial protection of second window after L-NAME pretreatment is related to the activation of adenosine A1 receptor. Methods Thirty Sprague-Dawley rats were randomly divided into 3 groups (10 rats in each group): Ischemia control group, L-NAME pretreatment group and antagonist group. Each group was given Langendorff perfusion The changes of HR, LVDP and CF were observed at S15, R1, R60 and R120 time points after 60 min of reperfusion and 120 min of reperfusion. The cTnI level in coronary effluent was measured. Microstructure changes. Results There was no difference in heart rate before ischemia in all groups. Compared with L-NAME group, the heart rate of the antagonist group was slower than that of L-NAME group (P <0.05), and there was no difference with ischemic control group. LVDP Compared with the L-NAME pretreatment group, the difference was statistically significant (P <0.05), and there was no difference with the ischemic control group; the CF of the antagonist group was less than that of the L-NAME pretreatment group, the difference was statistically (P <0.05), but there was no difference with the ischemic control group. The cTnI of antagonist group was significantly higher than that of L-NAME pretreatment group (P <0.05), but no difference with ischemic control group Compared with the L-NAME preconditioning group, the myocardial ultrastructure damage in the blood control group was heavier. Conclusions Adenosine A1 receptor antagonist DPCPX blocks the protective effect of L-NAME on the second window. Adenosine A1 receptor may play a protective role in myocardial protection induced by L-NAME pretreatment.