We observed that both low and high doses of H2O2 (100 microM 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 H2O2, especially at the 1 mM dose. Most remarkable were the increases in the intensity of the phosphomonoester resonance that occurred immediately after exposure to H2O2. The major phosphomonoester species accumulating in hearts exposed to 1 mM H2O2 appears to be AMP. Exposure of hearts to H2O2 in the setting of metabolic acidosis did not significantly alter the functional response of isolated hearts to H2O2. However, the increases in phosphomonoester peak intensity following both doses of H2O2 and the decreases in tissue ATP and total phosphates following 1 mM H2O2 were attenuated by metabolic acidosis.
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