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机构地区:[1]重庆医科大学临床学院麻醉科,重庆400016 [2]中国医学科学院阜外医院麻醉体外循环研究室,北京100037
出 处:《重庆医科大学学报》2001年第4期407-409,415,共4页Journal of Chongqing Medical University
摘 要:目的:研究缺血预处理(IPC)对兔未成熟心肌缺血再灌注损伤的影响,并探讨其可能机制。方法:利用Langendorff模型灌注幼兔(14—21天)离体心脏。18只幼兔心随机分为2组,每组9只IPC组经历5min缺血、10min再灌的IPC处理后,使用 St. ThomasⅡ心麻痹液(STH)使心脏停跳;对照组只用 STH停跳心脏。两组兔心均在生理体温(39℃)下接受 45min缺血、40min灌注。观察复灌后的心肌酶释放、心肌能量、心脏功能及病理学变化。结果:与对照组相比,IPC组肌酸磷酸激酶同工酶(CK-MB)漏出量明显减少(P<0 .01),心肌 ATP含量以保存(P<0. 05),再灌注末心脏左室发展压(LVDP)显著改善(P<0. 05);光、电镜显示经过缺血预处理的心肌细胞损伤轻。结论:缺血预处理能明显减轻兔未成熟心肌缺血再灌注损伤,改善再灌注后心脏功能的恢复,其机制可能与保存再灌注后心肌细胞中ATP含量有关。Objective: To investigate whether immature hearts experiencing global ischemia and reperfusion injury could be protected by ischemic preconditioning( IPC) and probe the possible mechanism. Methods : Aerobically perfused in Langendorff mode at 39t ,isolated immature rabbit hearts( 14 -21 days old)were subjected to a IPC stimulus consisting of 5 minutes of global ischenmia plus 10 minutes of reperfusion. This was followed by 45 minutes of global ischemia and 40 minutes of reperfusion. Left ventricular developed pressure( LVDP) , change of myocardial enzyme (CK - MB) in the coronary effluent, myocardial energy metabolism and morphology were de termined. Cold crystalloid cardioplegia was used to cause the hearts to arrest before the prolonged global I/R. Re sults : The LVDP value in IPC group was significantly higher than that in control. The CK - MB leakage in IPC group was decreased significantly (24.58 ± 5.09 U/L versus 32.80 ± 5.32 U/L in controls P<0. 01). The myocardial levels of ATP in preconditioned group at the end of the reperfusion was significantly preserved(208. 14 ±24. 2ug /g versus 174.52 ± 15. 69ugg/g in controls P<0. 05). Light and electron microscopic findings of myocardium showed the preconditioned hearts were less severely damaged. Conclusion : IPC has a protective effect on the immature rabbit hearts suffering from global I /R injury,which is possibly connected with the preservation of ATP level in myocardium tissue.
分 类 号:R542.2[医药卫生—心血管疾病]
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