1，6－二磷酸果糖和卡托普利抗心肌缺血和再灌注损伤的实验研究

Experimental Study of Protective Effects of Fructose-1.6-Diphosphate and Captopril on Myocardial Ischemia and Reperfusion Iujury

在离体大鼠心脏灌流模型上，探讨了心肌缺血再灌注损伤机制，同时比较了１，６－二磷酸果糖（ＦＤＰ）和卡托普利（ＣＰ）对心肌缺血再灌注损伤的保护作用。结果表明：（１）ＦＤＰ和ＣＰ对缺血心肌和再灌注损伤均有保护效果，但ＦＤＰ仅在缺氧开始给药，才能充分发挥其效应；二者联合用药对心肌保护有更好的效果。（２）缺血损伤的严重程度决定着再灌注损伤的程度，改善缺氧影响是防止再灌注损伤的先决条件。

An experimental study on the effects of fructose-1 .6-diphosphate(FDP) and Captopril(CP) on myocardial protection was performed by utilizing the isolated perfused working rat heart model. The mechanism of myocardial reperfusion injury was discussed. Results indicated: 1. FDP and CP could significantly reduce the reperfusion injury, but the protective effect of FDP could only be fully exerted when it was administered at the beginning of ischemia rather than during reperfusion. Administration of FDP combined with CP could provide better protective effects during the period of the ischemia. 2. Myocardial reperfusion injury was related directly to the preexisting myocardial ischemic injury. Minimizing the ill effects of anoxia could play an important role in preventing reperfusion inJury.