To elucidate the difference in the mechanisms for alkalization during ischemic
acidosis between diabetic and non-diabetic hearts, intracellular pH (pHi) was measured by
phosphorus-31 magnetic resonance spectroscopy. Diabetes was induced by the injection of
streptozotocin. The accumulation of
proton ion (DeltaH+) during 15 min global
ischemia at 37 degreesC was calculated from pH i. There were no significant differences in DeltaH+ between diabetic (DM: 0. 54+/-0.03 micromol/l,n=6; mean+/-s.e.m.) and non-DM hearts (0.57+/-0.04, n=6), when perfused with
bicarbonate buffer. However, perfusion with
HEPES buffer revealed a significant increase of DeltaH+ in DM (0.85+/-0.07, n=5) compared with non-DM (0.61+/-0.06, n=5P<0.05). On the contrary, the addition of a Na+/H+ exchange inhibitor (
EIPA; 1 micromol/l) to
bicarbonate buffer significantly increased DeltaH+ in non-DM (1.09+/-0.10, n=4) compared with DM (0.71+/-0.03, n=5P<0.01). Perfusion with
HEPES buffer and
EIPA equally increased DeltaH+ in both groups (DM 1.13+/-0.13, n=4; non-DM 1.15+/-0.14, n=4). Thus, the activity of Na+/H+ exchanger during ischemic
acidosis, assessed as the increase of DeltaH+ induced by addition of
EIPA to
bicarbonate buffer, was higher in non-DM (0.52) than DM (0.17). In contrast, the contribution of
bicarbonate-dependent systems evaluated by the deference of DeltaH+ between the
bicarbonate buffer and the
HEPES buffer was markedly bigger in DM (0.31) than non-DM (0.04). These results indicate that Na+/H+ exchange is a major mechanism to compensate ischemic
acidosis in non-DM hearts, whereas
bicarbonate-dependent systems compensate the depressed activity of Na+/H+ exchange in DM.