Circulation Research, Vol 70, 1091-1098, Copyright © 1992 by American Heart Association

ARTICLES

Effect of cyclooxygenase blockade on blood flow through well-developed coronary collateral vessels

J Altman, D Dulas and RJ Bache
Department of Medicine, University of Minnesota Medical School, Minneapolis.

Collateral vessels that develop after coronary artery occlusion demonstrate perivascular inflammation, subintimal hyperplasia, and endothelial proliferation. This study was performed to test the hypothesis that these abnormalities are associated with evidence for increased production of vasodilator prostaglandins. Eight dogs were studied 4-6 months after occlusion of the anterior descending coronary artery had been performed to stimulate collateral vessel growth. At the time of study, the anterior descending coronary artery was cannulated at the site of occlusion to allow measurement of retrograde blood flow as an index of interarterial collateral flow. Injection of radioactive microspheres during the retrograde flow collection allowed determination of continuing tissue flow in the collateral-dependent zone as an index of intramural microvascular collateral flow. Retrograde and tissue flows were measured before and 20 minutes after 5 mg/kg i.v. indomethacin, a dose that caused 95 +/- 3% inhibition of the coronary vasodilation in response to a 500 micrograms intracoronary bolus of arachidonic acid. Heart rate and mean aortic pressure were not significantly altered by indomethacin, and blood flow to the normally perfused myocardial region was not changed by administration of indomethacin. However, indomethacin caused a 40 +/- 7% decrease in retrograde flow (p less than 0.01), and microvascular collateral flow to the dependent myocardium decreased by 20 +/- 10% (p less than 0.05). These data indicate that, unlike the normal coronary circulation, well- developed coronary collateral vessels are under the tonic influence of vasodilator prostaglandins.

This article has been cited by other articles:

				D. J. Duncker and R. J. Bache Regulation of Coronary Blood Flow During Exercise Physiol Rev, July 1, 2008; 88(3): 1009 - 1086. [Abstract] [Full Text] [PDF]

				D. Merkus, B. Houweling, A. Zarbanoui, and D. J. Duncker Interaction between prostanoids and nitric oxide in regulation of systemic, pulmonary, and coronary vascular tone in exercising swine Am J Physiol Heart Circ Physiol, March 1, 2004; 286(3): H1114 - H1123. [Abstract] [Full Text] [PDF]

				J. R. Kersten, W. G. Toller, J. P. Tessmer, P. S. Pagel, and D. C. Warltier Hyperglycemia reduces coronary collateral blood flow through a nitric oxide-mediated mechanism Am J Physiol Heart Circ Physiol, November 1, 2001; 281(5): H2097 - H2104. [Abstract] [Full Text] [PDF]

				K. L. Griffin, M. H. Laughlin, and J. L. Parker Exercise training improves endothelium-mediated vasorelaxation after chronic coronary occlusion J Appl Physiol, November 1, 1999; 87(5): 1948 - 1956. [Abstract] [Full Text] [PDF]

				J. H. Traverse, D. Judd, and R. J. Bache Dose-Dependent Effect of Endothelin-1 on Blood Flow to Normal and Collateral-Dependent Myocardium Circulation, February 1, 1996; 93(3): 558 - 566. [Abstract] [Full Text]