The direct in vivo effects of nitric oxide on the coronary
circulation.
Chambers, Jeffrey W., Gregory S. Voss, Jason R. Snider, Susan M.
Meyer, Julie L. Cartland, and Robert F. Wilson.
Cardiovascular Division, Department of Medicine, University of
Minnesota, Minneapolis, Minnesota
APStracts 3:0086H, 1996.
To determined the direct in vivo effects of 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 [mu]mol) caused a step-wise increase in CBFV (3.1+/-0.3 x basal
CBFV at 8 [mu]mol) similar to adenosine (2.6+/-0.3 x basal CBFV,
maximal dose). Continuous subselective infusions (0.1,1.0 and 4.0
[mu]mol/min) caused dose-dependent increases in CBFV (2.2+/-0.3 x
basal CBFV at 4.0 [mu]mol/min) and epicardial artery diameter (+15+/
-6 % diameter). Left main infusions (8 [mu]mol/min) caused a step wise
increase in CBFV and 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
nitric oxide 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.
Received 27 July 1995; accepted in final form 16 February 1996.
APS Manuscript Number H709-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 March 96