Effect of acidosis on hydrogen peroxide injury to the isolated perfused rat heart
Evans, T.; Jin, H.; Elkins, N.; Shapiro, J.I.
American Journal of Physiology 269(1 Pt 2): H308-H312
1995
ISSN/ISBN: 0002-9513 PMID: 7631862 Document Number: 445591
We observed that both low and high doses of H-2O-2 (100 mu-M and 1 mM, respectively) caused significant and irreversible injury to cardiac contractile function in the isolated perfused heart model. Using 31P-nuclear magnetic resonance spectroscopy, we observed marked metabolic changes following exposure to H-2O-2, especially at the 1 mM dose. Most remarkable were the increases in the intensity of the phosphomonoester resonance that occurred immediately after exposure to H-2O-2. The major phosphomonoester species accumulating in hearts exposed to 1 mM H-2O-2 appears to be AMP. Exposure of hearts to H-2O-2 in the setting of metabolic acidosis did not significantly alter the functional response of isolated hearts to H-2O-2. However, the increases in phosphomonoester peak intensity following both doses of H-2O-2 and the decreases in tissue ATP and total phosphates following 1 mM H-2O-2 were attenuated by metabolic acidosis.