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.