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目的 :观察心肌缺血预处置和再灌注损伤时心肌内源性 1 1 ,1 2 -环氧二十碳三烯酸 (1 1 ,1 2 -epoxye icosatrienoicacid ,1 1 ,1 2 -EET)的改变 ,探讨内源性 1 1 ,1 2 -EET在缺血预处置中的作用。方法 :使用雄性Wistar大鼠 ,通过结扎 (60min)和松开 (30min)冠状动脉左前降支 ,复制心肌缺血 /再灌注模型 ;采用缺血 5min ,再灌注 5min两次造成缺血预处置。实验分 5组 :①假手术组 (sham) ;②缺血再灌注组 (I/R) ;③短阵缺血预处置组 (SI) ;④短阵缺血预处置缺血 /再灌注组 (SI+I/R)。采用气相色谱法测定心肌 1 1 ,1 2 -EET的含量 ,并观察再灌注过程中心功能的变化。结果 :I/R组 +dp/dtmax、-dp/dtmax以及LVDP均低于、心肌 1 1 ,1 2 -EET高于sham组及SI +I/R组 (P <0 0 1 ) ;而SI+I/R组心肌 1 1 ,1 2 -EET也高于sham组 (P <0 0 1 )。结论 :整体动物心肌再灌注使大量内源性 1 1 ,1 2 -EET释放 ,是再灌注损伤机制之一 ;缺血预处置抑制再灌注时心肌 1 1 ,1 2 -EET的增加 ,可能与缺血预处置心肌保护作用有关。
OBJECTIVE: To observe the changes of myocardial endogenous 1 1, 1 2-epoxyeicosatrienoic acid (1 1, 1 2 -EET) in myocardial ischemic preconditioning and reperfusion injury Change, to explore the role of endogenous 1 1, 1 2 -EET in ischemic preconditioning. Methods: Myocardial ischemia / reperfusion model was established by ligating the left anterior descending coronary artery (60min) and releasing the left anterior descending branch (30min) in male Wistar rats. Ischemic preconditioning was induced by ischemia 5min and reperfusion 5min. The experiment was divided into 5 groups: sham group, ischemia / reperfusion group (I / R), short segment ischemic preconditioning group (SI), ischemia / reperfusion group (SI + I / R). The content of myocardial 1 1, 1 2 -EET was determined by gas chromatography and the changes of cardiac function during reperfusion were observed. Results: The levels of dp / dtmax, -dp / dtmax and LVDP in I / R group were both lower than those in sham group and SI + I / R group (P <0.01) + I / R group myocardial 1 1, 1 2 -EET also higher than the sham group (P <0.01). CONCLUSION: Whole body myocardial reperfusion can release a large amount of endogenous 1 1, 1 2 -EET, which is one of the mechanisms of reperfusion injury. Ischemia preconditioning can inhibit the increase of myocardial 1 1, 1 2 -EET during reperfusion, Ischemic preconditioning of myocardial protection.