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目的 :评价线粒体三磷酸腺苷敏感性钾通道 (mitoKATP)开放剂二氮嗪 (diazoxide ,Diaz)对大鼠心肌缺血损伤的保护作用。 方法 :选用Wistar大鼠 3 6只 ,分为对照组 8只、异丙肾上腺素 (ISO)组 10只、二氮嗪 10mg/kg组 9只和二氮嗪2 0mg/kg组 9只。用ISO 5mg/kg皮下注射复制大鼠心肌缺血损伤模型 ,2 4h后采血测定血清乳酸脱氢酶 (LDH)和肌酸激酶 (CK)活性及乳酸含量 ,同时监测心电图、血压和心率的变化 ,并观察心肌组织形态学改变。 结果 :ISO引起大鼠心肌缺血损伤时 ,ISO组与对照组比较 ,血清LDH、CK活性和乳酸含量明显增加 ,有极显著性差异 (P <0 0 1) ,组织形态学也发生明显改变 ,心肌细胞损伤严重 ,有极显著性差异 (P <0 0 1)。预先口服二氮嗪 10～ 2 0mg/kg可逆转血清LDH、CK和乳酸的升高 ,有显著性差异 (P <0 0 5～ 0 0 1) ,减轻心肌细胞损伤程度。二氮嗪 10mg/kg不影响收缩压和心率。 结论 :二氮嗪对ISO诱发的大鼠心肌缺血损伤具有保护作用
AIM: To evaluate the protective effect of diazoxide (diaz), a mitochondria ATP sensitive potassium channel (mitoKATP) opener, on myocardial ischemia in rats. Methods: 36 Wistar rats were randomly divided into control group (n = 8), isoproterenol (ISO group), diazoxide 10 mg / kg group and diazoxide 20 mg / kg group. The model of myocardial ischemia injury was induced by subcutaneous injection of ISO at a dose of 5 mg / kg. Serum lactate dehydrogenase (LDH), creatine kinase (CK) activity and lactate content were determined by blood sampling 24 hours later. The changes of electrocardiogram, blood pressure and heart rate , And observed myocardial tissue morphological changes. Results: Compared with the control group, the serum LDH and CK activities and the content of lactic acid in ISO group increased significantly (P <0.01) and the histomorphology also changed significantly , Severe myocardial cell injury, there was a significant difference (P <0.01). Pre-oral diazoxide 10 ~ 20mg / kg can reverse serum LDH, CK and lactic acid increased significantly (P <0 05 ~ 0 0 1), reduce the degree of myocardial cell injury. Diazoxide 10 mg / kg did not affect systolic blood pressure and heart rate. Conclusion: Diazoxide has a protective effect on myocardial ischemia induced by ISO in rats