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目的探讨压力超负荷大鼠肥厚心肌线粒体内膜 ADP/ATP 载体(AAC)转运活性的变化。方法将雄性 SD 大鼠随机分为假手术组和腹主动脉缩窄组,术后5周及15周观察大鼠血流动力学参数、心室重构指标,密度梯度离心法提取大鼠心肌线粒体,用抑制剂终止法测定线粒体 AAC 的转运活性,高效液相色谱法测量心肌线粒体内腺苷酸含量。结果大鼠腹主动脉缩窄术后5周出现左心室肥厚,术后15周加重伴心功能减退;术后5周 AAC 活性降低,但无统计学意义,15周时 AAC 活性显著减低与线粒体内(ATP+ADP)含量下降相一致。结论压力超负荷后心功能减退的肥厚心肌 AAC 转运活性降低,使能量产生和利用异常,提示 AAC 活性改变是肥厚心肌组织能量代谢障碍及心功能减退的重要机制。
Objective To investigate the changes of mitochondrial ADP / ATP carrier (AAC) transport in hypertrophic myocardium of hypertensive rats. Methods Male Sprague-Dawley rats were randomly divided into sham operation group and abdominal aorta constriction group. The hemodynamic parameters, ventricular remodeling index and density gradient centrifugation were used to extract rat myocardial mitochondria at 5 and 15 weeks after operation , The mitochondrial AAC transporter activity was determined by the inhibitor termination method, and the content of adenosine monophosphate in myocardial mitochondria was measured by high performance liquid chromatography. Results Left ventricular hypertrophy occurred at 5 weeks after abdominal aorta constriction in rats and aggravated with cardiac dysfunction at 15 weeks after operation. AAC activity decreased at 5 weeks after operation, but there was no statistical significance. AAC activity was significantly decreased at 15 weeks (ATP + ADP) content decreased consistent. Conclusions The AAC transport activity of hypertrophic myocardium after pressure overload is decreased and the energy production and utilization are abnormal. It is suggested that the alteration of AAC activity is an important mechanism of energy metabolism and cardiac dysfunction in hypertrophic myocardium.