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作 者:郑理玲[1] 陈良才[1] 吴伟平[1] 陈宏伟[1] 张志孟[1]
机构地区:[1]福建医科大学附属泉州第一医院心外科,泉州362000
出 处:《中华胸心血管外科杂志》2013年第3期169-171,共3页Chinese Journal of Thoracic and Cardiovascular Surgery
基 金:福建省医学创新课题(2012-CXB-45);泉州市科技研究课题(2012215)
摘 要:目的探讨心肌胰岛素抵抗在心肌缺血致心力衰竭发生发展中的作用机制。方法雄性sD大鼠48只,随机数字表法分为对照组和心肌梗死心力衰竭组,每组24只,冠状动脉左前降支缝扎术建立心肌缺血致心力衰竭模型。在离体心脏灌注工作试验中,测定葡萄糖和脂肪酸的氧化率及其在胰岛素刺激下的变化情况。实验结束时取心肌组织以免疫蛋白印迹杂交法检测p38MAPK的蛋白表达。结果心肌梗死后导致心脏明显扩张、射血分数下降(〈0.50)。在基础状态下心肌葡萄糖氧化正常,但脂肪酸氧化显著减低。胰岛素对底物氧化的作用明显受损,表现为胰岛素刺激下葡萄糖氧化增加的程度和脂肪酸氧化降低的程度都显著下降。心肌梗死心衰组与对照组相比,心肌p38MAPK的蛋白表达明显下降(P〈0.05)。结论大鼠心肌梗死引起局部的底物氧化水平的胰岛素抵抗,心肌细胞p38MAPK表达下降。心肌胰岛素抵抗与线粒体受损和心脏收缩功能障碍有关,调节p38MAPK表达可能是其分子生物学基础之一。Objective This study was carried out to investigate the effect of myocardial insulin resistance on expression of p38 mitogen-activated protein kinase (MAPK) in ischemie heart failure in rat. Methods Male sprague-dawley rats were subjected either to ligation of the left anterior descending artery (LAD) ( n = 24 ) or to sham operation ( n = 24 ). After two weeks, cardiac size and function were determined by echocardiography. Glucose and fatty acid (FAO) oxidation rates as well as insulin response were measured in the isolated working heart. The protein expression of p38MAPK was evaluated by Western blotting. Results The infarcted hearts were dilated and had a reduced ejection fraction (ejection fraction 〈 0. 50). The basal glucose oxidation was preserved, but the fatty acid oxidation was significantly reduced. Insulin effect on substrate oxidation was significantly impaired for both the decrease in fatty acid oxidation and the increase in glucose oxidation. The protein expression of p38 MAPK in infracted hearts wasfisigni cantly reduced ( P 〈 0.05 ). Conclusion Myocardial infarction in rats caused par- tial insulin resistance at the level of substrate oxidation, which was associated with cardiac contractile dysfunction and the ex- pression of p38MAPK.
关 键 词:心肌 胰岛素 心力衰竭P38MAPK 心肌胰岛素抵抗
分 类 号:R541.6[医药卫生—心血管疾病]
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