Paradoxical effect of ischemic preconditioning on ischemic contracture? NMR studies of energy metabolism and intracellular pH in the rat heart.

Using the blood-perfused rat heart, we have previously shown that although ischemic preconditioning (PC) and cardioplegia (CP) afforded similar protection against post-ischemic contractile dysfunction this effect was not additive even though PC accelerated whereas CP delayed ischemic contracture. Using NMR we examined the effects of these interventions on pHi and ATP metabolism during global ischemia. Isolated rat hearts (n = 6/group) with an intraventricular balloon were aerobically perfused with buffer, subjected to zero flow ischemia (37 degrees C) for 35 min and reperfused for 40 min. The groups were: (1) controls without protection, (2) PC (2 cycles), and (3) St Thomas' cardioplegia, prior to test ischemia. PC accelerated whereas CP delayed ischemic contracture (P < 0.05 v controls). Yet, after 40 min reperfusion, both interventions produced substantial improvements in the recovery of LVDP (P < 0.05 v controls). During 35 min ischemia, the decline of ATP was delayed by CP but accelerated by PC (P < 0.05 v controls). The pHi fell steeply in controls to a plateau of 5.9 after 14 min ischemia. PC had no effect on the rate of fall of pHi but reduced its extent (P < 0.05). CP delayed the onset of the decline in pHi (P < 0.05) but, once initiated, there was no effect on the rate of decline to a plateau. Thus, despite protecting post-ischemic contractile function, PC accelerated ischemic contracture and the depletion of ATP, but substantially reduced intracellular acidosis. In contrast, CP slowed ischemic contracture and the depletion of ATP; it also delayed the onset of acidosis.