Intracellular lactate controls adenosine output from canine
gracilis muscle during moderate systemic hypoxia.
Mo, F. M., & H. J. Ballard.
The Department of Physiology, The University of Hong Kong, Hong
Kong
APStracts 3:0321H, 1996.
The influence of systemic hypoxia on lactate and adenosine output from
isolated, constant-flow perfused gracilis muscle was determined in
anesthetized dogs. The lactate-transport inhibitor, [alpha]-cyano-4
-hydroxycinnamic acid (CHCA) was employed to distinguish the direct
effects of hypoxia on adenosine output from those produced indirectly
by changing lactate concentration. Reduction of arterial Po2 from 135
+/- 4 to 39 +/- 2 mmHg raised arterial lactate from 1.26 +/- 0.32 to
2.22 +/- 0.45 mM, but decreased (V-A) lactate from 0.53 +/- 0.09 to
-0.13 +/- 0.19 mM, indicating that lactate output was abolished from
the muscle. Arterial adenosine did not change, but V-A adenosine
increased from 20.6 +/- 10.1 to 76.5 +/- 14.4 nM. CHCA infusion
during hypoxia abolished adenosine output from gracilis muscle (V-A
adenosine = -20.5 +/- 40.6 nM). In isolated rat soleus muscle fibers,
intracellular pH increased from 6.96 +/- 0.04 to 7.71 +/- 0.14 in
response to a reduction of Po2 from 459 +/- 28 to 53 +/- 3 mmHg.
Correspondingly, adenosine output decreased from 3.71 +/- 0.15 to
3.04 +/- 0.27 nM. These data suggest that hypoxia did not directly
stimulate adenosine output from red oxidative skeletal muscle, but
rather, systemic hypoxia increased lactate delivery, and the
resulting increase in intracellular lactate decreased pHi, which
stimulated adenosine output.
Received 12 September 1995; accepted in final form 18 July 1996.
APS Manuscript Number H857-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 21 August 1996