PRECONDITIONING AND HYPOTHERMIC CARDIOPLEGIA PROTECT HUMAN HEART EQUALLY AGAINST ISCHEMIA

Background. The purpose of this study was to determine whether transie nt ischemic preconditioning protects human myocardium against normothe rmic ischemic injury. Methods. Isolated human right atrial trabeculae were suspended in an organ bath with oxygenated Tyrode's solution at 3 7 degrees C and field stimulated at 1 Hz. Developed force was recorded . Trabeculae (Warm I/R) received normoxic perfusion before 45 minutes of normothermic simulated ischemia (hypoxic, substrate-free buffer wit h pacing at 3 Hz) and 120 minutes of reperfusion. Preconditioned trabe culae (Warm IPC) were subjected to 5 minutes of normothermic simulated ischemia and 10 minutes of perfusion before normothermic simulated is chemia-reperfusion injury. Trabeculae (Cold I/R) were subjected to hyp othermic (4 degrees C) ischemia (hypoxic buffer) for 4 hours and 60 mi nutes of reperfusion (37 degrees C). Preconditioned trabeculae (Cold I PC) were pretreated with 5 minutes of normothermic simulated ischemia before hypothermic ischemia and 60 minutes of reperfusion. At the end of reperfusion, trabeculae were frozen at -70 degrees C and assayed fo r tissue creatine kinase activity. Results. At the end of reperfusion, warm preconditioned trabeculae (Warm IPC) recovered 51% +/- 5% of bas eline developed force, whereas warm I/R trabeculae recovered 24% +/- 3 % (p < 0.05). Tissue creatine kinase levels reflecting preserved tissu e viability were sustained in Warm IPC trabeculae (1,183 +/- 204 U/g), whereas nonpreconditioned control trabeculae (Warm I/R) exhibited low er levels of enzymatic activity (403 +/- 32 U/g) (p < 0.05). In contra st, Cold IPC trabeculae recovered 47% +/- 5% and Cold UR, 56% +/- 8% o f baseline developed force at the end of reperfusion (p > 0.05). Concl usions. We conclude that transient ischemic preconditioning protects h uman myocardium against normothermic ischemic injury. (C) 1997 by The Society of Thoracic Surgeons