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Thromboxane Contributes to Submaximal Coronary Dilation During Myocardial Ischemia
Author(s) -
ELLER BRIAN T.,
BROOKS LEONARD A.,
DELLSPERGER KEVIN C.
Publication year - 1995
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.3109/10739689509146764
Subject(s) - cardiology , medicine , constriction , coronary arteries , microcirculation , thromboxane a2 , coronary perfusion pressure , coronary vessel , stenosis , coronary circulation , vasodilation , vasoconstriction , thromboxane , ischemia , anesthesia , hemodynamics , platelet , blood flow , artery , cardiopulmonary resuscitation , resuscitation
Objectives: Thromboxane has been shown to contribute to coronary constriction in conduit coronary arteries during platelet aggregation at the site of a critical stenosis. Previous studies from our laboratory suggest that following a critical coronary stenosis, persistent vasomotor tone occurs. We tested the hypothesis that thromboxane is responsible for that increased tone. Methods: To test this hypothesis, 14 mongrel dogs of either sex were anesthetized and subjected to a critical coronary stenosis where distal coronary perfusion pressure was reduced to 36 ± 2 mm Hg. During the coronary stenosis, SQ 29,548 (thromboxane/endoperoxide receptor antagonist) was administered intravenously (0.2 mg/kg and 2.0 mg/kg). Coronary microvascular responses were observed by directly visualizing the epicardial microcirculation. Diameters were measured using intravital microscopy coupled to stroboscopic epi‐illumination and jet ventilation to compensate for cardiac and respiratory‐induced motion. Results: Coronary microvessels were divided into small (< 150 μm) and large (> 150 μm) arterioles. During SQ 29,548 administration, small coronary arterioles demonstrated no additional dilation during a critical coronary stenosis. In contrast, coronary microvessels > 150 μm demonstrated a dose‐dependent vasodilation to SQ 29,548 (0.2 mg/kg: 6 ± 2%; 2.0 mg/kg: 11 ± 4%; P < 0.05 vs. no change). A time control study in six additional animals demonstrated no significant coronary microvascular diameter changes following a critical stenosis over the time course of SQ 29,548 administration. Conclusion: Endoperoxides contribute to poststenotic microvascular vasoconstriction in vessels 150–300 μm.