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本研究用离体兔心灌注模型比较内皮源性超极化因子（ＥＤＨＦ）与内皮源性舒张因子（Ｅ－ＤＲＦ即一氧化氮）和前列环素（ＰＧＩ２）的特性。（１）注人缓激肽（Ｂｋ３～３０００ｐｍｏｌ／Ｌ）产生剂量依赖性扩张反应，以冠状动脉灌注压（ＣＰＰ）下降及舒张持续时间表示。（２）联合应用ＮＯ合酶及ＰＧＩ２合成酶抑制剂Ｎ－亚硝基－Ｌ－精氨酸（ＬＮＮＡ，０．３ｕｍｏｌ／Ｌ）和ｄｉｃｌｏｆｅｎａｃ（１０ｕｍｏｌ／Ｌ），Ｂｋ引起的冠状动脉舒张反应时相明显缩短（Ｐ＜０．０５～０．００１），而ＣＰＰ降低无明显改变（Ｐ＞０．０５）。（３）上述基础上加用钾通道阻滞剂－阿帕明（１ｕｍｏｌ／Ｌ），结果Ｂｋ引起的ＣＰＰ下降及冠状动脉舒张反应时间均被显著抑制（Ｐ＜０．０５或Ｐ＜０．０１），且该抑制用灌流方法清除阿帕明后解除。（４）应用ＬＮＮＡ－ｄｉｃｌｏｆｅｎａｃ基础上，阿帕明对ＥＤＲＦ类似物—Ｓ－亚硝基－Ｌ－半胱氨酸（１ｎｍｏｌ／Ｌ）引起的ＣＰＰ下降及扩张反应时相均无明显影响（Ｐ＞０．０５）。（５）依次应用ＬＮＮＡ、ｄｉｃｌｏｆｅｎａｃ和阿帕明，基础ＣＰＰ分别提高２９％、８％和６０％。本研究结果提示：①Ｂｋ引起兔冠状动脉阻力血管扩张；②Ｂｋ触发的非Ｅ?
In this study, the characteristics of endothelium-derived hyperpolarizer (EDHF) and endothelium-derived relaxing factor (E-DRF) and prostacyclin (PGI2) were compared with isolated rabbit heart perfusion model. (1) Bk3 ~ 3000 pmol / L injected dose-dependent dilatation reaction, which was expressed as the decrease of coronary perfusion pressure (CPP) and the duration of diastole. (2) Combined application of NO synthase and PGI2 synthase inhibitor N-nitroso-L-arginine (LNNA, 0.3umol / L) and diclofenac (10umol / L), Bk-induced coronary vasodilation (P <0.05 ~ 0.001), while there was no obvious change in CPP (P> 0.05). (3) Adding potassium channel blocker (1 μmol / L) based on the above results showed that the decrease of CPP and the relaxation time of coronary artery were significantly inhibited by Bk (P <0.05 or P <0. 01), and the inhibition was removed by apheresis following perfusion. (4) On the basis of LNNA-diclofenac, APMP had no significant effect on the CPP decline and dilation phase induced by EDRF analogue S-nitroso-L-cysteine (1nmol / L) > 0.05). (5) The application of LNNA, diclofenac and apamin in turn, the basic CPP increased by 29%, 8% and 60% respectively. The results of this study suggest that: ①Bk caused by rabbit coronary artery resistance vasodilation; ② Bk triggered non-E?