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, andDepartment of Physiology and Biophysics and Center for Bioengineering, University of Washington, Seattle, Washington 98195-7290
Adenosine has been postulated to mediate the
increase in coronary blood flow when myocardial oxygen consumption is
increased. The aim of this study was to evaluate the role of adenosine
when myocardial oxygen consumption was augmented by cardiac
paired-pulse stimulation without the use of catecholamines. In 10 anesthetized closed-chest dogs, coronary blood flow was measured in the
left circumflex coronary artery, and myocardial oxygen consumption was
calculated using the arteriovenous oxygen difference. Cardiac interstitial adenosine concentration was estimated from coronary venous
and arterial plasma adenosine measurements using a previously described
multicompartmental, axially distributed mathematical model. Paired
stimulation increased heart rate from 55 to 120 beats/min, increased
myocardial oxygen consumption 104%, and increased coronary blood flow
92%, but the estimated interstitial adenosine concentration remained
below the threshold for coronary vasodilation. After adenosine-receptor
blockade with 8-phenyltheophylline (8-PT), coronary blood flow and
myocardial oxygen consumption were not significantly different from
control values. Paired-pulse pacing during adenosine-receptor blockade
resulted in increases in myocardial oxygen consumption and coronary
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 is not required for the local metabolic control of coronary
blood flow during pacing-induced increases in myocardial oxygen consumption.
canine; 8-phenyltheophylline; hyperemia
Deceased 15 July 1997.
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