ROLE OF ADENOSINE IN VASODILATION OF EPIMYOCARDIAL CORONARY MICROVESSELS DURING REDUCTION IN PERFUSION-PRESSURE

Previous studies in which an isolated heart or in situ constant pressu re preparation was used suggested a minimal role for adenosine in auto regulatory control of coronary circulation. These results, however, ar e controversial, and the role of adenosine in autoregulation of flow i n heart is uncertain. To test the hypothesis that adenosine mediates m icrovascular dilation in response to reduction in perfusion pressure ( PP), we performed experiments in 41 open-chest chloralose-anesthetized dogs. Internal diameters (ID) of epicardial small arterioles < 100 mu m were measured with an intravital microscope and stroboscopic epiill umination synchronized to cardiac cycle. PP was reduced by graded sten oses of the left anterior descending coronary artery (LAD, mild stenos is PP = 60 mm Hg; critical stenosis PP = 40 mm Hg) and complete occlus ion. 8-Phenyltheophylline (8-PT 10 mu M) or adenosine deaminase (ADA 1 0 U/min) was topically superfused onto the heart. Arteriolar dilation induced by topically applied adenosine less than or equal to 10 mu M w as completely blocked by 8-PT. Without 8-PT (vehicle group), mild crit ical stenosis and complete occlusion caused arteriolar dilation (perce ntage of change in diameter 8.6 +/- 2.6, 16.0 +/- 2.7, and 13.6 +/- 4. 8%). 8-PT did not inhibit this dilation (8.5 +/- 2.8, 16.1 +/- 4.6, 15 .1 +/- 5.7%, NS vs, vehicle group). Topically applied ADA significantl y inhibited intravenously (i.v.) administered adenosine-induced arteri olar dilation. Without ADA, arteriolar dilation occurred (16.6 +/- 3.0 , 28.2 +/- 4.3, 15.4 +/- 6.2%, at each PP). However, ADA did not inhib it dilation induced by gradual stenoses (10.6 +/- 1.4, 24.2 +/- 4.3, 1 7.5 +/- 6.9%, at each PP, NS vs. vehicle group). These data indicate t hat adenosine does not play a primary role in autoregulatory or ischem ia-induced coronary microvascular dilation.