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本工作用放射免疫法、荧光组织化学等方法探讨心肌儿茶酚胺和前列环素在大鼠缺血再灌注心律失常发生中的作用。结扎左冠状动脉造成局部心肌缺血然后再灌注。在缺血再灌注组，缺血再灌注引起的心室纤颤发生率为７８％；在巯甲丙脯酸组，巯甲肉脯酸预处理可使缺血再灌注心室纤颤发生率下降了６５．５％；与缺血再灌注组相比，巯甲丙脯酸组的心肌儿茶酚胺含量、心肌６－酮－ＰＧＦ；。（６－Ｋｅｔｏ－ＰＧＦ１α）的含量明显升高（Ｐ＜０．０１），血栓素Ｂ２（ＴｘＢ２）的含量和ＴｘＢ２／６Ｋｅｔｏ－ＰＧＦ１α的比值则明显降低（Ｐ＜０．０１）。在ＡｕｇⅡ组，ＡｎｇⅡ灌流可逆转巯甲丙脯酸的保护作用，使心室纤颤发生率升高至８５％，心肌儿茶酚胺的含量与缺血再灌注组无显著性差异（Ｐ＞０．０５）。上述结果表明，巯甲丙脯酸可显著降低缺血再灌注引起的心室纤颤发生率，这种作用可能是由于抑制了ＡｕｇⅡ的生成，减少心肌儿茶酚胺的释放以及抑制ＴｘＡ２的生成和促进ＰＧＩ２的合成。
This work by radioimmunoassay, fluorescence histochemistry and other methods of myocardial catecholamines and prostacyclin in rat ischemia-reperfusion arrhythmia in the role. Ligation of the left coronary artery causes local myocardial ischemia followed by reperfusion. In ischemia-reperfusion group, the incidence of ventricular fibrillation caused by ischemia-reperfusion was 78%. In captopril group, captopril pretreatment decreased the incidence of ventricular fibrillation after ischemia-reperfusion 65.5%; myocardial catecholamine content, myocardial 6-keto-PGF in captopril group compared with ischemia-reperfusion group. (P <0.01). The contents of TxB2 and TxB2 / 6Keto-PGF1α were significantly decreased (P <0.01). In Aug Ⅱ group, Ang Ⅱ perfusion could reverse the protective effect of captopril and increase the incidence of ventricular fibrillation to 85%. There was no significant difference in myocardial catecholamines between ischemia and reperfusion group (P> 0.05) . The above results indicate that captopril can significantly reduce the incidence of ventricular fibrillation induced by ischemia-reperfusion, which may be due to inhibition of Aug II production, decrease of cardiac catecholamine release, inhibition of TxA2 production and promotion of PGI2 synthesis.