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Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, Washington 98195-7290
The role of
ATP-sensitive K+ (KATP+) channels, nitric
oxide, and adenosine in coronary exercise hyperemia was investigated. Dogs (n = 10) were chronically instrumented with
catheters in the aorta and coronary sinus and instrumented with a flow
transducer on the circumflex coronary artery. Cardiac interstitial
adenosine concentration was estimated from arterial and coronary venous plasma concentrations using a previously tested mathematical model. Experiments were conducted at rest and during graded treadmill exercise
with and without combined inhibition of KATP+ channels
(glibenclamide, 1 mg/kg iv), nitric oxide synthesis (N
-nitro-L-arginine, 35 mg/kg
iv), and adenosine receptors (8-phenyltheophylline, 3 mg/kg iv). During
control exercise, myocardial oxygen consumption increased ~2.9-fold,
coronary blood flow increased ~2.6-fold, and coronary venous oxygen
tension decreased from 19.9 ± 0.4 to 13.7 ± 0.6 mmHg.
Triple blockade did not significantly change the myocardial oxygen
consumption or coronary blood flow response during exercise but lowered
the resting coronary venous oxygen tension to 10.0 ± 0.4 mmHg and
during exercise to 6.2 ± 0.5 mmHg. Cardiac adenosine levels did
not increase sufficiently to overcome the adenosine receptor blockade.
These results indicate that combined inhibition of
KATP+ channels, nitric oxide synthesis, and adenosine
receptors lowers the balance between total oxygen supply and
consumption at rest but that these factors are not required for local
metabolic coronary vasodilation during exercise.
coronary blood flow; exercise; myocardial oxygen consumption
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