Effects of ischemic preconditioning on long-time heart preservation

本研究旨在评价缺血预处理对心脏冷藏液长期保存的药理保护作用。先前的研究表明，蛋白激酶C（PKC）的激活可以保护离体大鼠心肌细胞免受缺血和再灌注损伤。缺血前心肌细胞中PKC的激活可减轻心肌细胞的Ca2+超载，有助于减少心肌凋亡。我们用离体大鼠心脏灌注模型（Langendorff）检验了CPK是否同样的机制在长时间心脏保存中发挥作用。短期缺血再灌注（各5min：预处理）后，用St.Thomas溶液（心脏停搏液）诱导离体大鼠心脏骤停，4℃下分别在3种保存液（St.Thomas溶液、UW溶液、生理盐水溶液）中保存120、240min。通过比较缺血预处理后左心室收缩力（LVDP: mmHg, LVDP /dT max）、舒张功能（LVEDP: mmHg, LVDP /dT min）、心率（HR: /min）等指标，得出缺血预处理后左心室保护功能增强的指标。但三种溶液的心脏功能无显著差异。这些数据表明，缺血预处理的心脏保护可能有效地促进心脏移植过程中供体心脏的保存。由于技术问题，我们未能估计心脏保存的药理学影响和teromeaze活性的关系。

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.