Role of adenosine in local metabolic coronary vasodilation

Citation
T. Yada et al., Role of adenosine in local metabolic coronary vasodilation, AM J P-HEAR, 45(5), 1999, pp. H1425-H1433
Citations number
44
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
ISSN journal
03636135 → ACNP
Volume
45
Issue
5
Year of publication
1999
Pages
H1425 - H1433
Database
ISI
SICI code
0363-6135(199905)45:5<H1425:ROAILM>2.0.ZU;2-T
Abstract
Adenosine has been postulated to mediate the increase in coronary blood flo w when myocardial oxygen consumption is increased. The aim of this study wa s to evaluate the role of adenosine when myocardial oxygen consumption was augmented by cardiac paired-pulse stimulation without the use of catecholam ines. In 10 anesthetized closed-chest dogs, coronary blood flow was measure d in the left circumflex coronary artery, and myocardial oxygen consumption was calculated using the arteriovenous oxygen difference. Cardiac intersti tial adenosine concentration was estimated from coronary venous and arteria l plasma adenosine measurements using a previously described multicompartme ntal, axially distributed mathematical model. Paired stimulation increased heart rate from 55 to 120 beats/min, increased myocardial oxygen consumptio n 104%, and increased coronary blood flow 92%, but the estimated interstiti al adenosine concentration remained below the threshold for coronary vasodi lation. After adenosine-receptor blockade with 8-phenyltheophylline (8-PT), coronary blood flow and myocardial oxygen consumption were not significant ly different from control values. Paired-pulse pacing during adenosine-rece ptor blockade resulted in increases in myocardial oxygen consumption and co ronary blood flow similar to the response before 8-PT. Coronary venous and estimated interstitial adenosine concentration did not increase to overcome the adenosine blockade by 8-PT. These results demonstrate that adenosine i s not required for the local metabolic control of coronary blood flow durin g pacing-induced increases in myocardial oxygen consumption.