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目的：通过观察细胞色素ｐ４５０抑制剂对大鼠在体心肌缺血／再灌注损伤的影响，了解细胞色素ｐ４５０与心肌缺血／再灌注损伤的关系，并初步分析作用机制。方法：观察给予细胞色素ｐ４５０抑制剂或１１，１２－ＥＥＴ后，大鼠在体心肌缺血／再灌注室性心律失常、心肌梗塞范围及超微结构的变化，及ＴＥＡ与ｇｌｉｂｅｎｃｌａｍｉｄｅ对ＥＥＴｓ作用的影响。结果：细胞色素ｐ４５０抑制剂ｃｌｏｔｒｉｍａｚｏｌｅ（０．９ｍｍｏｌ／Ｌ）和ＳＫＦ５２５Ａ（０．５４ｍｍｏｌ／Ｌ）减轻、而外源性１１，１２－ＥＥＴ加重缺血／再灌注心律失常、心肌梗塞范围及心肌超微结构病变；ＴＥＡ与ｇｌｉｂｅｎｃｌａｍｉｄｅ可拮抗１１，１２－ＥＥＴ的作用。结论：细胞色素ｐ４５０参与了心肌缺血／再灌注损伤；其作用与ＥＥＴｓ释放并开通钙敏感性及ＡＴＰ敏感性钾通道有关。
OBJECTIVE: To investigate the effect of cytochrome p450 inhibitor on myocardial ischemia / reperfusion injury in rats and to investigate the relationship between cytochrome p450 and myocardial ischemia / reperfusion injury and its mechanism of action. Methods: The changes of ventricular arrhythmia, infarct size and ultrastructure in myocardial ischemia / reperfusion in rats after administration of cytochrome p450 inhibitor or 11,12-EET and the effect of TEA and glibenclamide on EETs were observed influences. Results: Cytochrome p450 inhibitor clotrimazole (0.9 mmol / L) and SKF525A (0.54 mmol / L) alleviated, while exogenous 11,12-EET increased ischemia / reperfusion arrhythmia, myocardial infarction and myocardial ultrasonography Microstructure lesions; TEA and glibenclamide can antagonize the role of 11,12-EET. CONCLUSION: Cytochrome p450 is involved in myocardial ischemia / reperfusion injury. Its function is related to the release of EETs and activation of calcium-sensitive and ATP-sensitive potassium channels.