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Thromboxane contributes to submaximal coronary dilation during myocardial ischemia
B T Eller1, L A Brooks, K C Dellsperger
1Department of Internal Medicine, University of Iowa, Iowa City 52242, USA.
Microcirculation (New York, N.Y. : 1994)
|August 1, 1995
Summary
Thromboxane contributes to coronary artery constriction after stenosis. Blocking thromboxane receptors with SQ 29,548 dilated larger coronary microvessels, indicating its role in vasoconstriction.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
Background:
- Thromboxane contributes to coronary artery constriction during platelet aggregation at critical stenosis sites.
- Previous research suggests persistent vasomotor tone occurs after critical coronary stenosis.
Purpose of the Study:
- To test the hypothesis that thromboxane is responsible for increased vasomotor tone following critical coronary stenosis.
Main Methods:
- 14 mongrel dogs underwent critical coronary stenosis, reducing distal perfusion pressure.
- SQ 29,548 (thromboxane/endoperoxide receptor antagonist) was administered intravenously at 0.2 and 2.0 mg/kg.
- Coronary microvascular responses were visualized using intravital microscopy.
Main Results:
- Small coronary arterioles (<150 microns) showed no dilation with SQ 29,548.
- Larger microvessels (>150 microns) exhibited dose-dependent vasodilation (6-11%) in response to SQ 29,548.
- Control studies confirmed no significant microvascular changes over time.
Conclusions:
- Endoperoxides contribute to vasoconstriction in poststenotic microvessels (150-300 microns).
- Thromboxane receptor antagonism leads to vasodilation in larger coronary microvessels after stenosis.