AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 271: H1584-H1593, 1996;
0363-6135/96 $5.00
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AJP - Heart and Circulatory Physiology, Vol 271, Issue 4 1584-H1593, Copyright © 1996 by American Physiological Society

ARTICLES

Direct in vivo effects of nitric oxide on the coronary circulation

J. W. Chambers, G. S. Voss, J. R. Snider, S. M. Meyer, J. L. Cartland and R. F. Wilson
Department of Medicine, University of Minnesota, Minneapolis 55455, USA.

To determine the direct in vivo effects of nitric oxide (NO) on the coronary circulation, we infused NO-saturated saline (1.0 +/- 0.1 mmol/l) into the coronary arteries of anesthetized dogs and measured changes in coronary blood flow velocity (CBFV) with a Doppler catheter, changes in coronary artery size with quantitative angiography, and transmural myocardial perfusion with radioactive microspheres. Boluses of NO (1-8 micromol) caused a stepwise increase in CBFV (3.1 +/- 0.3 x basal CBFV at 8 micromol) similar to that caused by adenosine (2.6 +/- 0.3 x basal CBFV, maximal dose). Continuous subselective infusions (0.1, 1.0, and 4.0 micromol/min) caused dose-dependent increases in CBFV (2.2 +/- 0.3 x basal CBFV at 4.0 micromol/min) and in epicardial artery diameter (+ 15 +/- 6% diam). Left main infusions (8 micromol/min) caused a stepwise increase in CBFV and in the endocardial-to-epicardial flow ratio without affecting systemic hemodynamics. Brief infusion of NO (2 min) did not significantly reduce acetylcholine-mediated endothelial NO release. Therefore, despite rapid metabolism, direct intra-arterial infusion of NO can be given at a rate sufficient to overwhelm metabolic elimination, providing direct evidence that NO is a potent in vivo coronary vasodilator. Moreover, the enhanced subendocardial vasodilator response to direct NO infusion suggests increased regional sensitivity to NO.


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