Nonischemic myocardial hypoxia: coronary dilation without increased tissue adenosine.

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.