Effect of acidosis on hydrogen peroxide injury to the isolated
perfused rat heart.
Evans, T., H. Jin, N. Elkins, and J. I. Shapiro.
University of Colorado School of Medicine. Denver, Colorado, The
Giles Filley Research Laboratory and Departments of Medicine and
Radiology, Webb Waring Lung Institute and University of Colorado
School of Medicine
APStracts 2:0104H, 1995.
We observed that both low and high doses of H2O2 (100 [mu]M and 1 mM,
respectively) caused significant and irreversible injury to cardiac
contractile function in the isolated perfused heart model. Using 31P
NMR 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
which occurred immediately after exposure to H2O2. The major
phosphomonester species accumulating in hearts exposed to 1 mM H2O2
appears to be adenosine monophosphate. 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.
Received 12 August 1994; accepted in final form 6 February 1995.
APS Manuscript Number H726-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 4 April 1995.