加强心脏直视手术心肌保护作用的研究
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摘要
本实验在离体大鼠心脏灌流模型上,探讨了心肌在缺血再灌注时的损伤机理,观察了左心室功能、心肌钙离子含量、心肌细胞超微结构的改变和酶释放的变化;同时比较了1.6-二磷酸果糖[FDP]和硫甲丙脯酸[CAP]对心肌缺血再灌注损伤的保护作用,实验分为六组,每组8只大鼠心脏。1.对照组:心脏在常温下(37±0.5℃)停搏20分钟,然后再灌注35分钟;2.再灌开始给药组(共二组):在再灌注液中分别加FDP和CAP;3.缺血开始给药组(共三组):在缺血开始分别给FDP和CAP及FDP+CAP,实验结果发现:对照组再灌注期心功能明显受到损伤,且心脏舒张功能改变较其收缩功能的改变出现早而明显;细胞内钙离子超负荷;LDH释放增加,再灌注期给药,FDP对左室收缩功能指标呈负性反应,保护心肌效果明显比CAP差(P<0.05)。CAP在再灌注期或缺血开始给药,两组对心肌均有非常显著保护效果(P<0.01),两组之间相比较无显著差别,而在缺血开始给药FDP保护心肌效果明显提高,不仅明显优于再灌注期间给药组,而且非常显著优于CAP两组(P<0.01)。心肌超微结构,心肌细胞酶LDH释放和心肌细胞钙离子含量亦呈一致性反应。实验结果表明:1.FDP和CAP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;FDP和CAP二者联合用药对缺血心肌的保护和防止再灌注损伤比单一用药有更大
Experimental study of protective effects of Fructose -1.6-Diphosphate (FDP) and Captopril(CAP) on myocardial ischemial reperfusion injury.
    utilizing the isolated perfused working rat heart model, the mechanism and protective effects of myocardial ischemial reperfusion injury on left ventricular function, myocardial ca~(?) content, lactic dehydrogenase[LDH) and myocardial ultrastructure were studied. There were six groups for study and 8 rat heart in each group in this experiment: (1) control group: Cardial arrest for 20 min under normothrmal(37±0.5℃) and reperfusion for 35 min; (2) Grorp of drug administration during the reperfusion: There Were two subgroup, in this groups, FDP_1(perfusate Contained FDP)and CAP_1(perfusate containced Captopril.) (3) Group of drug administration from the beginning of ischemia There were three subgroups in this group, namely FDP_2. CAP_2 and FDP_2 + CAP_2. In these subgroups the drugs above-mentioned added to the perfusate respectively.The results showed: In the control group, the cardiac function deteriorated significantly, the change of left ventricular function in diastolic phase was earlier and more obvious than that in the systolic phase. The myocardial ca~(?) content and the LDH release increased significantly, in the subgroup FDP, the index of left ventricle contraction were nective reaction. The Protective effecf of FDP on myocardium was lowere than that of CAP. in subgroup CAP_1 as well as in CAP_2. In these two CAP subgroups the significant protective effect on myocardium was observed and there was no significant difference between them. The more significant protective effect on myocardial uitrastructure. LDH resease and ca~(?) content appeared in the subgroup FDP_2 and the result in subgroup FDP_2 was better than that not only in subgroup FDP_1 but also in subgroup CAP_1 and CAP_2. Results indicated: 1. FDP and CAP could signficatly reduce the reperfusion injury, but, the much protective effect of FDP was only administered at the beginning of ischemia other than of reperfusion. Administration of FDP Combined With CAP could provide better Protective effects during the period of the ischemia. 2. myocardial reperfusion injury was related directly to the myocardial ischemis injury. Improving anoxia Could Play an important role in preventing reperfusion injury.
引文
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