利多氟嗪的心肌保护作用机制－腺苷转运抑制

The Myocardial Protective Mechanism of Lidofiazine:Adenosine Transport Inhibition

用１８只狗研究了利多 嗪（Ｌｉｄｏｆｌａｚｉｎｅ）的心肌保护作用机制。实验分三组：对照组（Ｃ）、利多 嗪组（Ｌ）及利多 嗪加氨茶硷组（ＬＡ）。在体外循环（ＥＣＣ）开始前１５分钟内给予实验药物及安慰剂。然后施行四次间断升主动脉阻断１５分钟间隔以１０分钟再灌注。ＥＣＣ结束后监测６０分钟心功能恢复情况。结果发现在最后一次主动脉阻断未Ｌ组心肌腺苷含量是Ｃ组的３．５倍；每次再灌注时Ｌ组心肌腺苷释放量远较Ｃ组高：Ｌ组心肌摄取乳酸盐量每次再灌注时都恢复到正常水平，而Ｃ组则没有恢复正常；Ｌ组心功能各项指标的恢复均明显优于Ｃ组。当用了腺苷受体阻滞剂氨茶硷后再用利多嗪时，其心肌保护作用明显下降，而心肌腺苷的含量及释放量在Ｌ组与ＬＡ组间无明显差异。

The myocardial protective mechanism of lidoflazine was investigated in l8 dogs which were divided into three groups:Control(C),Lidoflazine(L)and Lidoflzine plus aminophyline(LA)groups,All hearts were subjected to four times of 15 minutes of global ischemia separated by 10 reperfusion. Myocardial adenosine content of L group was 3.5 times of that in the C group at the end of the last aortic crossclamping.The release of adenosine from the myocardium during each reperfusion period was significantly higher than that in the C group。Myocardial extraction of lactate was normalized at every reperfusion interval in the L group but not in the C group.In the L group,cardiac function was significantly better than that in the C group at 60 minutes after extracorporeal circulation, When the adenosine receptor blocker aminophyline was used before the use Of lidoflazine,myocardial protection dropped significantly.