Thromboxane Contributes to Submaximal Coronary Dilation During Myocardial Ischemia

BRIAN T. ELLER, LEONARD A. BROOKS, Kevin C Dellsperger

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

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. 1995 Blackwell

Original languageEnglish (US)
Pages (from-to)165-172
Number of pages8
JournalMicrocirculation
Volume2
Issue number2
DOIs
StatePublished - Jan 1 1995

Fingerprint

Coronary Stenosis
Thromboxanes
Myocardial Ischemia
Dilatation
Arterioles
Microvessels
Pathologic Constriction
Thromboxane Receptors
Microcirculation
Vasoconstriction
Platelet Aggregation
Constriction
Vasodilation
Ventilation
Coronary Vessels
Perfusion
Dogs
Pressure

Keywords

  • Coronary microcirculation
  • SQ 29,548
  • coronary stenosis
  • endothelin
  • intravital microscopy
  • ischemia
  • thromboxane

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Thromboxane Contributes to Submaximal Coronary Dilation During Myocardial Ischemia. / ELLER, BRIAN T.; BROOKS, LEONARD A.; Dellsperger, Kevin C.

In: Microcirculation, Vol. 2, No. 2, 01.01.1995, p. 165-172.

Research output: Contribution to journalArticle

ELLER, BRIAN T. ; BROOKS, LEONARD A. ; Dellsperger, Kevin C. / Thromboxane Contributes to Submaximal Coronary Dilation During Myocardial Ischemia. In: Microcirculation. 1995 ; Vol. 2, No. 2. pp. 165-172.
@article{f3ce87bfb45a461c8c5ecba8c683f0fd,
title = "Thromboxane Contributes to Submaximal Coronary Dilation During Myocardial Ischemia",
abstract = "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. 1995 Blackwell",
keywords = "Coronary microcirculation, SQ 29,548, coronary stenosis, endothelin, intravital microscopy, ischemia, thromboxane",
author = "ELLER, {BRIAN T.} and BROOKS, {LEONARD A.} and Dellsperger, {Kevin C}",
year = "1995",
month = "1",
day = "1",
doi = "10.3109/10739689509146764",
language = "English (US)",
volume = "2",
pages = "165--172",
journal = "Microcirculation",
issn = "1073-9688",
publisher = "Wiley-Blackwell",
number = "2",

}

TY - JOUR

T1 - Thromboxane Contributes to Submaximal Coronary Dilation During Myocardial Ischemia

AU - ELLER, BRIAN T.

AU - BROOKS, LEONARD A.

AU - Dellsperger, Kevin C

PY - 1995/1/1

Y1 - 1995/1/1

N2 - 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. 1995 Blackwell

AB - 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. 1995 Blackwell

KW - Coronary microcirculation

KW - SQ 29,548

KW - coronary stenosis

KW - endothelin

KW - intravital microscopy

KW - ischemia

KW - thromboxane

UR - http://www.scopus.com/inward/record.url?scp=0029349049&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029349049&partnerID=8YFLogxK

U2 - 10.3109/10739689509146764

DO - 10.3109/10739689509146764

M3 - Article

VL - 2

SP - 165

EP - 172

JO - Microcirculation

JF - Microcirculation

SN - 1073-9688

IS - 2

ER -