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Department of Surgery, University of Colorado, Denver, Colorado 80262
Ischemic preconditioning (PC) attenuates cardiac
acidosis during global ischemia. This adaptation to
ischemia is detectable before other better known indexes of PC
are manifested. Clarification of the endogenous mechanisms may provide
insights into how protein kinase C (PKC) signaling might be linked to
altered intracellular biochemistry.
31P NMR studies of isolated, buffer-perfused rat heart
were performed to determine whether functionally cardioprotective PC by
cyclic ischemia (CI) and
1-adrenergic stimuli
[phenylephrine (PE)] attenuated acidosis during
ischemia and, if so, whether this
1) involves a PKC-dependent pathway
and is due to 2) decreased
glycolytic proton production, 3) an
increase in proton buffering, or 4)
proton extrusion. At the end of 20 min of global ischemia, both
CI-PC (pH = 6.86 ± 0.14) and PE-PC (pH = 6.90 ± 0.13)
attenuated end-ischemic acidosis (control pH = 6.54 ± 0.1). PKC
blockade with chelerythrine (Chel) prevented the attenuation of
ischemic acidosis by PC stimuli (end-ischemic pH: CI + Chel,
6.43 ± 0.06; PE + Chel, 6.17 ± 0.17). End-ischemic lactate
accumulation was decreased in CI-PC hearts (7.54 ± 0.5 vs. control,
14.61 ± 2.1 µmol/g wet wt) but not in those preconditioned
through the 1-adrenergic
receptor (12.25 ± 0.9 µmol/g wet wt). Physiologically relevant
buffers were not increased in the preconditioned groups. Blockade of
the
Na+/H+
exchanger [NHE; with
5-(N-ethyl-N-isopropyl)
amiloride (EIPA) or HOE-694] eliminated the attenuation of
ischemic acidosis seen with PC stimuli (pH: CI + EIPA, 6.5 ± 0.1;
PE + EIPA, 6.46 ± 0.2; PE + HOE-694, 6.26 ± 0.15; not
significantly different from control). We conclude that CI and
1-adrenergic PC stimuli
attenuate ischemic acidosis, and this may involve the cardiac
amiloride-sensitive NHE. The signaling pathways of both these two
stimuli appear to involve PKC.
myocardial ischemia; myocellular acidosis; sodium/hydrogen
exchange; 31P nuclear magnetic
resonance spectroscopy; cyclic ischemic preconditioning; 1-adrenergic agonist; phenylephrine
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