Circulation, Vol 76, 952-959, Copyright © 1987 by American Heart Association
JH Ashton, ML Ogletree, IM Michel, P Golino, JM McNatt, AL Taylor, S Raheja, J Schmitz, LM Buja and WB Campbell
We have reported previously that thromboxane A2/prostaglandin (PG)H2 and
serotonin independently mediate the occurrence of cyclic flow variations
(CFVs) in a canine preparation of severe coronary artery narrowing. This
may be due to an effect of these substances on platelets and/or the
vascular wall. We tested the hypothesis that there is a cooperative effect
between thromboxane A2/PGH2 and serotonin receptor stimulation in the
development of CFVs in this animal preparation. After placement of a hard
plastic cylindrical constrictor around the left anterior descending
coronary artery, CFVs develop and are characterized by repetitive cycles of
declines in coronary blood flow and abrupt increases in flow. In a control
group of dogs, CFV frequency (cycles/hour) and severity (lowest coronary
blood flow just before its restoration) did not change significantly over a
3 hr interval. In a second group of dogs, CFVs were established after
constrictor placement, abolished with the serotonin (5HT2) receptor
antagonist ketanserin, and reestablished by the continuous infusion of
serotonin into the left atrium. Serotonin-induced CFVs were then abolished
with a thromboxane A2/PGH2 receptor antagonist, SQ29,548, or a thromboxane
synthetase inhibitor, dazoxiben (UK37,248). The relative specificity of the
respective antagonists, SQ29,548 and ketanserin, was determined in canine
platelets and rat aortic vascular strips. No significant cross-reactivity
between ketanserin and SQ29,548 was found. Thus, the data obtained in these
studies demonstrate a cooperative interaction between thromboxane A2/PGH2
and serotonin S2 receptors that contributes to the development of CFVs in
this experimental preparation.
ARTICLES
Cooperative mediation by serotonin S2 and thromboxane A2/prostaglandin H2 receptor activation of cyclic flow variations in dogs with severe coronary artery stenoses
Department of Internal Medicine (Cardiology Division), University of Texas Health Science Center at Dallas 75235-9047.
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