Circulation, Vol 79, 899-910, Copyright © 1989 by American Heart Association
TA Fischell, U Nellessen, DE Johnson and R Ginsburg
To determine whether balloon angioplasty can provoke arterial
vasoconstriction independent of platelet aggregation and neurogenic input,
we studied the spontaneous vasomotor effects of balloon dilatation in
isolated, perfused whole-vessel segments of rabbit aorta and pig carotid
artery. Freshly dissected rabbit thoracic aortas were mounted in a muscle
bath-perfusion chamber, perfused with physiologic saline solution at 70 mm
Hg, and allowed to equilibrate. The proximal or distal half of the aortas
were dilated with either a "large" (5 mm, 31-51% stretch beyond relaxed
diameter) or a "small" (4 mm, 5-16% stretch) balloon angioplasty catheter
with the other half of the vessel serving as the control. A similar series
of experiments were performed in pig carotid arteries using "large" (6 or 8
mm, 48-90% stretch) balloon catheters. The spontaneous vasomotor effects of
balloon angioplasty were examined with long-axis, high-frequency ultrasonic
imaging combined with computerized edge detection image processing to
measure changes in segmental internal vessel diameters. Additional
experiments were carried out in rabbit aortas to determine the roles of the
endothelium, extracellular calcium, indomethacin, ibuprofen, and
calcium-channel blockade in modulating angioplasty-induced
vasoconstriction. Significant arterial vasoconstriction was observed in the
balloon angioplasty segments after dilatation with 5-mm balloons but not
with 4-mm balloons. After dilatation with 5-mm balloons, the angioplasty
segments' cross-sectional areas decreased by an average of 31% versus 4%
for the nondilated (control) segments (p less than 0.0001). Similar
postangioplasty vasoconstriction was observed in the pig carotid arteries
(decrease in minimal vessel cross-sectional area of 41% [angioplasty
segment] versus 2% [control segment]) (p less than 0.005). This
angioplasty-induced vasoconstriction was prevented by endothelial
denudation before angioplasty, removal of extracellular calcium, and
pretreatment with indomethacin or ibuprofen. The vasoconstriction was only
partially inhibited by calcium channel blockade with verapamil. These
findings demonstrate that stretch- pressure-induced arterial
vasoconstriction may occur after balloon angioplasty, independent of
platelet aggregation and neurogenic input. This angioplasty-induced
vasoconstriction appears to be mediated by an endothelially derived
cyclooxygenase product(s).
ARTICLES
Endothelium-dependent arterial vasoconstriction after balloon angioplasty
Division of Cardiology, Stanford University Medical Center, California 94305.
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