Preconditioning and hypothermic cardioplegia protect human heart equally against ischemia

The purpose of this study was to determine whether transient ischemic preconditioning protects human myocardium against normothermic ischemic injury.

Isolated human right atrial trabeculae were suspended in an organ bath with oxygenated Tyrode's solution at 37 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 with pacing at 3 Hz) and 120 minutes of reperfusion. Preconditioned trabeculae (Warm IPC) were subjected to 5 minutes of normothermic simulated ischemia and 10 minutes of perfusion before normothermic simulated ischemia-reperfusion injury. Trabeculae (Cold I/R) were subjected to hypothermic (4 degrees C) ischemia (hypoxic buffer) for 4 hours and 60 minutes of reperfusion (37 degrees C). Preconditioned trabeculae (Cold IPC) 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 for tissue creatine kinase activity.

At the end of reperfusion, warm preconditioned trabeculae (Warm IPC) recovered 51% +/- 5% of baseline developed force, whereas warm I/R trabeculae recovered 24% +/- 3% (p < 0.05). Tissue creatine kinase levels reflecting preserved tissue viability were sustained in Warm IPC trabeculae (1,183 +/- 204 U/g), whereas nonpreconditioned control trabeculae (Warm I/R) exhibited lower levels of enzymatic activity (403 +/- 32 U/g) (p < 0.05). In contrast, Cold IPC trabeculae recovered 47% +/- 5% and Cold I/R, 56% +/- 8% of baseline developed force at the end of reperfusion (p > 0.05).

We conclude that transient ischemic preconditioning protects human myocardium against normothermic ischemic injury.