Circulation, Vol 86, 1302-1309, Copyright © 1992 by American Heart Association
SK Yao, JC Ober, A Krishnaswami, JJ Ferguson, HV Anderson, P Golino, LM Buja and JT Willerson
BACKGROUND. This study was designed to test the hypothesis that
endogenously produced nitric oxide protects against platelet aggregation
and cyclic flow variations in stenosed and endothelium- injured arteries of
mongrel dogs. METHODS AND RESULTS. NG-Monomethyl-L- arginine (L-NMMA), an
inhibitor of nitric oxide formation, was administered at 5 mg/kg to 15 dogs
after the left anterior descending coronary artery was mechanically injured
and narrowed by external constrictors and to nine dogs before endothelial
injury of the femoral artery and after injury and moderate arterial
constriction. Treatment with L-NMMA resulted in cyclic flow variations (as
detected by external Doppler flow probes) in the left anterior descending
artery of seven of 15 dogs and in the femoral artery of four of nine dogs
after endothelial injury. L-Arginine, the precursor for nitric oxide
synthesis, was administered at 60 mg/kg and abolished cyclic flow
variations in each of the 11 dogs. D-Arginine did not change the L-NMMA-
induced cyclic flow variations. Saline infusion did not induce or change
cyclic flow variations in any of the animals. Acetylcholine (1, 10, and 100
micrograms/min; n = 9) was administered in the femoral artery of nine
additional dogs before and after endothelial injury in moderately stenosed
femoral arteries. Acetylcholine did not induce cyclic flow variations in
any animal; however, it did increase the severity of cyclic flow variations
that developed in severely stenosed arteries. The diameter of the femoral
artery was measured by intravascular ultrasound imaging. L-NMMA caused
vasoconstriction of normal arteries, but no change was detected in
endothelium-injured arteries. In contrast, L-arginine caused vasodilation
of normal arteries, but, again, no change was noted in endothelium-injured
arteries. Acetylcholine dilated normal femoral arteries but constricted
arteries with endothelial injury. In both in vitro and ex vivo platelet
studies, L-NMMA enhanced platelet aggregation, whereas L-arginine
significantly reduced platelet aggregation. D-Arginine and acetylcholine
showed no effect on platelet aggregation. CONCLUSIONS. Promotion of nitric
oxide production decreases platelet aggregation and may eliminate cyclic
flow variations, whereas a reduction in nitric oxide formation enhances
platelet aggregation and may induce cyclic flow variations. Acetylcholine
causes vasoconstriction at the femoral arterial site of endothelial injury
and may increase the severity of cyclic flow variations.
ARTICLES
Endogenous nitric oxide protects against platelet aggregation and cyclic flow variations in stenosed and endothelium-injured arteries
Department of Cardiology Research, Texas Heart Institute, Houston.
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