To investigate the contribution of
acidosis to contractile dysfunction during early
myocardial ischemia, miniature intramyocardial pH
electrodes (0.2 mm tip diam) were used to correlate changes in extracellular pH (pHo) with tension in the isolated arterially perfused rabbit interventricular septum. A number of findings argue against
acidosis as the major cause of contractile failure during early
ischemia. During
hypoxia without
glucose present, the rate and pattern of tension decline was very similar to total
ischemia, suggesting that a common mechanism is involved. Throughout the initial period in which tension declined by 50%, however, pHo increased in the six of eight preparations during
hypoxia without
glucose. During
hypoxia with
glucose present, tension fell less rapidly than during
hypoxia without
glucose despite a significantly greater fall in pHo in the former case. The maximal rate of relaxation (-dT/dt) was markedly more sensitive to
ischemia,
hypoxia, or exposure to inhibitors of aerobic metabolism (
2,4-dinitrophenol and Na
azide) than the maximal rate of force development (+dT/dt). In contrast, +dT/dt and -dT/dt decreased almost symmetrically during exposure to
respiratory acidosis. During
ischemia, the change in pHo associated with 50% reduction in tension was 0.11 +/- 0.04 units. During
respiratory acidosis, this value was 0.45 +/- 0.02 units. From these observations we concluded that
acidosis is unlikely to be a major factor in the early decline of tension during
ischemia.