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在大鼠离体心脏观察了前列腺素介导缓激肽诱导的预适应对缺血再灌心肌的保护作用．３０ｍｉｎ缺血和３０ｍｉｎ再灌引起心功能降低（左室内压和左室内压最大上升速率下降），冠脉流量和心率降低以及肌酸激酶（ＣＰＫ）释放增加．缺血预适应（５ｍｉｎ缺血，５ｍｉｎ再灌，重复３次）能显著改善心功能，促进心率和冠脉流量的恢复，减少ＣＰＫ释放．其作用不受吲哚美辛（１０μｍｏｌ·Ｌ－１预先灌流３０ｍｉｎ）影响．预先用缓激肽（０．５μｍｏｌ·Ｌ－１）处理５ｍｉｎ产生缺血预适应样心肌保护作用，表现为促进心功能恢复，减少ＣＰＫ释放．该作用被预先灌流吲哚美辛取消．对照组，缺血再灌组，缓激肽组，吲哚美辛加缓激肽组的ＣＰＫ分别为（０．２８±０．０３），（２．２３±０．０６），（０．３９±０．０９），（１．８７±０．０５）μｍｏｌ·ｍｉｎ－１·ｇ－１湿组织．结果提示：缓激肽诱导预适应对缺血再灌心肌的保护作用与促前列腺素生成有关
Prostaglandin-mediated bradykinin-induced preconditioning was used to observe the protective effects of prostaglandin on myocardial ischemia-reperfusion in isolated rat hearts. 30min ischemia and 30min reperfusion led to decreased cardiac function (left ventricular pressure and maximum rate of decline in left ventricular pressure), decreased coronary flow and heart rate, and increased creatine kinase (CPK) release. Ischemic preconditioning (5min ischemia, 5min reperfusion, repeated 3 times) can significantly improve cardiac function, promote the recovery of heart rate and coronary flow, reduce the release of CPK. Its effect from indomethacin (10μmol·L-1 pre-perfusion 30min). Pretreatment with bradykinin (0.5μmol·L-1) for 5min resulted in ischemic preconditioning-like myocardial protection, which was shown to promote cardiac function recovery and reduce CPK release. This effect was ablated by indomethacin. The CPK of control group, ischemia reperfusion group, bradykinin group and indomethacin plus bradykinin group were (0.28 ± 0.03) and (2.23 ± 0.06) 39 ± 0.09), (1.87 ± 0.05) μmol · min-1 · g-1 wet tissue. The results suggest that bradykinin-induced preconditioning has a protective effect on prostaglandin production during myocardial ischemia / reperfusion