Experimental acidemia and muscle cell ph in chronic acidosis and
renal failure.
Bailey, James L, Brian K. England, Robert C. Long, Jr, Joseph
Weissman, and William E. Mitch.
Departments of Medicine, Renal Division, Neurology and the Fritz
Philips Magnetic Resonance Laboratory of Radiology, Emory University
School of Medicine, Atlanta, Georgia 30322
APStracts 2:0148C, 1995.
To test whether muscle cell pH (pHi) decreases when extracellular pH
falls, 31P NMR was utilized in rats made acidotic by infusing HCl,
gavage-feeding NH4Cl, or by inducing chronic renal failure (CRF). A 2
or 4 hour HCl infusion did not lower muscle pHi even though serum
bicarbonate fell to 5 mM. With chronic acidemia, blood pH was 7.15
+/- 0.01 versus 7.38 +/- 0.02 in pair-fed controls and muscle pHi was
7.09 +/- 0.01 and 7.14 +/- 0.02 respectively (P< 0.01). pHi in
muscle of CRF rats, (7.16 +/- 0.01) did not differ from sham
-operated, pair-fed controls (7.19 +/- 0.01) despite a blood pH of
7.23 +/- 0.05 in CRF versus 7.39 +/- 0.01 in controls. Since ion
transport is abnormal in CRF, we examined whether recovery of pHi is
impaired when muscles of six CRF and control rats were exercised to
tetany by stimulating the sciatic nerve. Neither pHi nor the recovery
of pHi differed between CRF and control rats. We conclude that pHi is
maintained in muscle in uremia and that signals other than changing
intracellular pH must be necessary to disrupt metabolism.
Received 27 December 1994; accepted in final form 9 March 1995.
APS Manuscript Number C738-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 28 March 1995.