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Effects of ischemic preconditioning on long-time heart preservation

缺血预处理对心脏长期保存的影响

基本信息

批准号：
15591474
负责人：
ISHIGURO Shingo
金额：
$ 2.24万
依托单位：
National University Corporation Tottori University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2003
资助国家：
日本
起止时间：
2003 至 2005
项目状态：
已结题

项目摘要

The present study designed to evaluate the effect of ischemic preconditioning and pharmacological protection for long time cardiac preservation in cold storage solutions. Previous findings suggest that the activation of protein kinase C(PKC) protects the myocardium from ischemia and reperfusion injury in isolated rat cardiomyocytes. The activation of PKC in cardiomyoctes before ischemia attenuates the Ca2+ overload of cardiomyocytes, in contributing to reduction of myocardial apoptosis. We examined whether the same mechanisms of CPK play a role in long time cardiac preservation with isolated rat heart perfusion model (Langendorff).After short term ischemia and reperfusion (each 5min : preconditioning), the isolated rat hearts were induced arrest with St.Thomas solution (cardioplegia) and were stored for 120 and 240min in 3 type preservation solutions (St.Thomas solution, UW solution and saline solution) at 4℃.On the basis of comparisons of postischemic left ventricular contractility (LVDP : mmHg, LVdP/dT max), diastolic function (LVEDP : mmHg, LVdP/dT min), heart rate (HR : /min), values indicative of improved protection were obtained by ischemic preconditiong. But, there was no significant difference in cardiac performances between 3 type solutions. These data suggest that cardioprotection by ischemic preconditioning might effectively contribute to improve donor heart preservation during cardiac transplantation.Due to technical problem, we failed to estimate about pharmacological influences in cardiac preservation and the relationship of the teromeaze activity.

本研究旨在评价缺血预处理和药物对长期低温保存心脏的保护作用。以往的研究表明，蛋白激酶C（PKC）的激活对大鼠心肌细胞缺血再灌注损伤具有保护作用。缺血前心肌细胞内PKC的激活可减轻心肌细胞内Ca ~（2+）超载，从而减少心肌细胞凋亡。本实验采用离体大鼠心脏灌流模型，探讨了CPK在长时间心脏保存中的作用机制在短期缺血和再灌注后，（每5分钟：用St.托马斯液诱导离体大鼠心脏停搏在3种保存液中保存120和240 min（St.托马斯液、UW液和生理盐水）在4℃下的左室收缩力比较通过缺血预处理，获得LVDP：mmHg，LVdP/dT max），舒张功能（LVEDP：mmHg，LVdP/dT min），心率（HR：/min），指示保护改善的值。但3种溶液的心脏性能无显著差异。这些数据表明，缺血预处理的心脏保护可能有助于改善心脏移植中供体心脏的保存。由于技术问题，我们未能估计心脏保存中的药理学影响和teromeaze活性之间的关系。