CsA对缺血再灌注心肌高能磷酸化合物代谢的影响  

Effect of ciclosporin A on high energy phosphates in rats with myocardial ischemia-reperfusion injury

作　　者：樊燕燕[1] 甄江涛[1] 朱宁[1] 赵晓丽[1] 曹颖[1] 王丽艳[1] 于公元[1] 张艳君[1] 

机构地区：[1]天津医科大学生物化学教研室,天津300070

出　　处：《天津医科大学学报》2011年第4期464-466,共3页Journal of Tianjin Medical University

摘　　要：目的:研究环孢素A(CsA)对大鼠心肌缺血再灌注损伤能量代谢的影响。方法:建立大鼠离体心肌缺血再灌注模型,测定心肌梗死面积,使用高效液相色谱(HPLC)法测定心肌组织中高能磷酸化合物ATP、ADP和AMP的含量,测定心肌组织Na+-K+-ATPase以及乳酸脱氢酶(LDH)活性,观察环孢素A(0.1 mg/mL)的保护作用。结果:环孢素A能显著降低缺血再灌注心脏灌流液的LDH水平,提高心肌组织ATP含量和能量物质的储备,降低心肌组织ATPase活性。结论:环孢素A对大鼠心肌缺血再灌注损伤有一定的保护作用。其作用机制可能与增加缺血区心肌能量物质含量,降低ATPase活性,改善能量代谢障碍有关。Objective： To study effect of ciclosporin A on energy metabolism in rats with myocardial ischemia- reperfusion injury. Methods： The ischemia-reperfusion model of rats was established by coronary artery ligation. The high energy phosphates（ATP, ADP and AMP） levels in myocardial tissue were measured by HPLC. The activities of the effluent of coronary artery lactate dehydrogenase（LDH）, supernatant ATPases and myocardial infarction size in myocardial tissue were assayed. Results： Ciclosporin A reduced the effluent of coronary artery LDH and myocardial infarction size, and significantly increased ATP concentrations and depressed the activities of Na＋- K＋-ATPase in injured myocardial tissue. Conclusion： Ciclosporin A protectes the myocardial tissues from the ischemia-reperfusion injury by depressed ATPase activities associated with energy metabolism.

关 键 词：环孢素A 缺血再灌注 能量代谢 大鼠 

分 类 号：Q5[生物学—生物化学] R542.22[医药卫生—心血管疾病]