Circulation, Vol 81, 1938-1947, Copyright © 1990 by American Heart Association
FW Sellke, JE Quillen, LA Brooks and DG Harrison
Previous in vivo studies have shown that vasopressin, which releases the
endothelium-derived relaxing factor and constricts coronary smooth muscle,
produces augmented constriction of coronary microvessels perfused by mature
collaterals. We hypothesized that chronic perfusion through collaterals
produces endothelial dysfunction in the recipient vasculature. Mature
collaterals were stimulated in mongrel dogs by the ameroid constrictor
technique. After 3-6 months, rings of conduit vessels (obtuse marginals)
were studied in organ chambers, and coronary microvessels (100-220 microns)
were studied in a pressurized, no-flow state with a microvessel imaging
apparatus. Eleven dogs were used as controls. Large vessels were
preconstricted with prostaglandin F2 alpha to 30-70% of the maximum
potassium chloride tension, and microvessels were preconstricted to 20-60%
of the baseline diameter with the thromboxane mimetic U46619. Relaxations
to the receptor-mediated agents acetylcholine and ADP were markedly
impaired in collateral-dependent coronary microvessels, whereas relaxations
to nitroglycerin were enhanced compared with microvessels from control
dogs. Relaxation to the calcium ionophore A23187, which releases the
endothelium-derived relaxing factor through nonreceptor-mediated
mechanisms, were similar in control and ameroid microvessels. Constriction
to vasopressin was augmented in collateral-dependent microvessels compared
with controls. Responses to all agonists were similar between control and
collateral- dependent large vascular rings. In conclusion, chronic
perfusion through collateral vessels selectively impairs receptor-mediated
endothelium-dependent relaxations and augments constriction to vasopressin
in the coronary microcirculation. These findings may have important
implications regarding neurohumoral regulation of perfusion to
collateral-dependent myocardium.
ARTICLES
Endothelial modulation of the coronary vasculature in vessels perfused via mature collaterals
Cardiovascular Center, University of Iowa College of Medicine, Iowa City.
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