Circulation, Vol 79, 154-166, Copyright © 1989 by American Heart Association
P Golino, JH Ashton, LM Buja, M Rosolowsky, AL Taylor, J McNatt, WB Campbell and JT Willerson
The goal of the present study was to demonstrate that intracoronary
platelet deposition may trigger intense vasoconstriction of large
epicardial coronary arteries in vivo and that this is largely mediated by
thromboxane A2 and serotonin released by activated platelets. Cyclic flow
variations (progressive declines in blood flow followed by sudden
restorations of flow) due to recurrent intracoronary platelet activation
and thrombus formation were induced by damaging the endothelium and placing
a cylindrical constrictor on the left anterior descending coronary artery
(LAD) in open-chest, anesthetized dogs. Coronary diameters were measured in
vivo by means of ultrasonic crystals sutured on the LAD immediately distal
to the constrictor (LAD1) and 1 cm below (LAD2) and on the circumflex
coronary artery (Cx). Coronary artery diastolic diameters were measured
continuously before and during cyclic flow variations and after they were
abolished by administration of LY53857, a serotonin-receptor antagonist
(group 1, n = 7), or SQ29548, a thromboxane-receptor antagonist (group 2, n
= 7). During cyclic flow variations, at the nadir of coronary flow, LAD1 (a
site of maximal platelet accumulation) cross-sectional area decreased by 52
+/- 10% and 38 +/- 6% in group 1 and 2 animals, respectively (p less than
0.001 compared with values recorded during a brief LAD occlusion obtained
by a suture snare), whereas LAD2 (a site of minimal or no platelet
accumulation) cross-sectional area did not differ from that recorded during
the brief LAD occlusion. SQ29548 abolished cyclic flow variations in seven
of seven dogs and LY53857 in six of seven, but they affected the increased
coronary vasoconstriction differently: LAD1 cross-sectional area increased
by 32 +/- 6% of the control value in SQ29548-treated animals, whereas it
returned to baseline dimension values in the LY53857-treated group as these
interventions also abolished the cyclic flow variations. We conclude that a
marked coronary vasoconstriction may be triggered by local platelet
deposition and that thromboxane A2 and serotonin are mediators of this
vasoconstriction.
ARTICLES
Local platelet activation causes vasoconstriction of large epicardial canine coronary arteries in vivo. Thromboxane A2 and serotonin are possible mediators
Department of Internal Medicine (Cardiology Division), University of Texas Southwestern Medical Center, Dallas 75235-9047.
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