AJP - Heart and Circulatory Physiology, Vol 243, Issue 4 512-H516, Copyright © 1982 by American Physiological Society
Nonischemic myocardial hypoxia: coronary dilation without increased tissue adenosine
H. F. Downey, G. J. Crystal, E. L. Bockman and F. A. Bashour
Experiments were performed in 23 open-chest, anesthetized dogs to evaluate
1) the extent of coronary vasodilation during nonischemic hypoxia and 2)
whether this dilation is associated with changes in cardiac concentrations
of adenosine, inosine, and hypoxanthine. Three minutes of nonischemic
myocardial hypoxia caused by selective perfusion of the left anterior
descending coronary artery (LAD) with hypoxic blood (PO2 = 11.7 Torr)
increased coronary flow 623%, an increase that was not significantly
different from that at the peak hyperemic response following 3 min of
ischemic hypoxia secondary to LAD occlusion (+534%). Concentrations for
adenosine and inosine (nmol/g) in myocardium sampled during nonischemic
hypoxia [0.8 +/- 0.2 (SE) and 0.8 +/- 0.2, respectively] were significantly
less than values during control conditions (1.7 +/- 0.3 and 1.4 +/- 0.2).
Hypoxanthine concentrations did not differ for nonischemic hypoxia and
control conditions. During ischemic hypoxia concentrations for adenosine
(31.2 +/- 4.9), inosine (91.0 +/- 13.6), and hypoxanthine (44.0 +/- 15.3)
were considerably greater than values during nonischemic hypoxia and during
control conditions. The results indicate that nonischemic hypoxia induced
pronounced coronary vasodilation similar to that during ischemic hypoxia,
with reduced rather than with increased tissue concentrations of adenosine
and inosine. These findings suggest that reduced myocardial oxygen tension
may cause dilation of coronary resistance vessels by a direct relaxant
effect on arteriolar vascular smooth muscle.
