Karck M, Rahmanian P, Haverich A
Department of Cardiovascular Surgery, University of Kiel, Germany.
Transplantation. 1996 Jul 15;62(1):17-22. doi: 10.1097/00007890-199607150-00004.
Ischemic preconditioning has not been assessed in an experimental model for myocardial preservation during heart transplantation. Using isolated working rat hearts, ischemic preconditioning was investigated as an adjunct to isolated hypothermic (group 1), crystalloid (group 2: University of Wisconsin solution; group 3: St. Thomas' Hospital cardioplegic solution II; group 4: Bretschneiders' cardioplegic solution), and noncrystalloid (group 5: cold blood cardioplegia) preservation during a 10-hr period of global ischemia at 4 degrees C. After acquisition of functional baseline data, ischemic preconditioning was induced with one cycle of 5 min of normothermic ischemia and 5 min of reperfusion before induction of global hypothermic ischemia (n= 10/group). Nonpreconditioned hearts (n= 10/group) were assessed for control. Ischemic preconditioning improved postischemic: functional recovery. Thus, aortic flow after 60 min of reperfusion recovered to 0%, 8%, 0%, 1% and 0% in control groups 1 to 5 without ischemic preconditioning and 21%, 25%, 10%, 8%, and 3% in groups 1 to 5 with ischemic preconditioning. The same pattern of recovery was observed in regard to postischemic maximum developed left ventricular pressure, which recovered to 21%, 56%, 30%, 36%, and 19% in groups 1 to 5 without preconditioning and 46%, 75%, 49%, 40%, and 47% in the corresponding groups with ischemic preconditioning. High-energy phosphate contents were not significantly different between preconditioned hearts and corresponding nonpreconditioned control hearts. Creatine kinase leakage during early reperfusion was found to be reduced with ischemic preconditioning. Thus, we have demonstrated that ischemic preconditioning can improve contractile function after global hypothermic ischemia in the isolated rat heart and we have shown that this protection is additive to that of hypothermia-induced protection during global ischemia at 4 degrees C. This endogenous mechanism of cardioprotection was effective regardless of whether preservation was accomplished using cardioplegic solution or topical hypothermia alone. This may have clinical implications in myocardial preservation for heart transplantation.
在心脏移植期间心肌保存的实验模型中，尚未对缺血预处理进行评估。使用离体工作大鼠心脏，研究了缺血预处理作为4℃下10小时全心缺血期间离体低温保存（第1组）、晶体液保存（第2组：威斯康星大学溶液；第3组：圣托马斯医院心脏停搏液II；第4组：布雷施奈德心脏停搏液）和非晶体液保存（第5组：冷血心脏停搏液）的辅助措施。在获取功能基线数据后，在诱导全心低温缺血之前，通过一个5分钟常温缺血和5分钟再灌注的周期诱导缺血预处理（每组n = 10）。评估未预处理的心脏（每组n = 10）作为对照。缺血预处理改善了缺血后的功能恢复。因此，在未进行缺血预处理的第1至5组对照组中，再灌注60分钟后的主动脉血流量恢复到0%、8%、0%、1%和0%，而在进行缺血预处理的第1至5组中分别恢复到21%、25%、10%、8%和3%。在缺血后最大左心室压力方面也观察到相同的恢复模式，在未预处理的第1至5组中分别恢复到21%、56%
