What question did this study set out to answer?

To determine the changes in endothelin-1 vascular reactivity and local endothelin release following coronary thrombosis, thrombolysis, and reperfusion in a porcine model.

November 1, 1995Journal of Cardiovascular Pharmacology

Myocardial Release of Endothelin (ET) and Enhanced ETA Receptor-Mediated Coronary Vasoconstriction After Coronary Thrombosis and Thrombolysis in Pigs

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Authors

QWQing‐Dong WangChina Animal Disease Control Center YUYozo UriudaNew Tokyo Hospital JPJohn PernowGeneral Cardiology

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Implication

Preclinical study reveals enhanced endothelin-1 vasoconstriction via ETA receptors after coronary thrombosis in pigs, suggesting a key driver of reperfusion injury and no-reflow.

Key Points

To determine the changes in endothelin-1 vascular reactivity and local endothelin release following coronary thrombosis, thrombolysis, and reperfusion in a porcine model.
Induced coronary thrombosis in pigs by deploying a copper coil in the left anterior descending coronary artery (LAD) and achieved reperfusion using tissue plasminogen activator (t-PA).
Evaluated in vitro vascular reactivity to endothelin-1 (ET-1), ETB receptor agonists, serotonin, and ETA antagonist BQ-123 in ischemic/reperfused versus nonischemic LAD diagonal branches.
Measured endothelin-like immunoreactivity (ET-LI) in paired plasma samples from the aorta and great cardiac vein to assess transmyocardial overflow during reperfusion.
Vasoconstrictor responses to ET-1 increased twofold (p < 0.01) in ischemic/reperfused arteries compared to nonischemic arteries, an effect mediated by ETA receptors and reversed by BQ-123.
Responses to ETB receptor agonists and serotonin were unchanged by ischemia/reperfusion, and NO synthase or cyclooxygenase inhibition did not alter ET-1 vasoconstriction.
Venoarterial concentration differences and coronary blood flow increased during reperfusion, significantly enhancing local myocardial overflow of ET-LI.

Cite This Study

Wang et al. (1995) studied this question.

synapsesocial.com/papers/6a6f17a4439bab0cabc2ae62 https://doi.org/10.1097/00005344-199511000-00014

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Implication

Preclinical study reveals enhanced endothelin-1 vasoconstriction via ETA receptors after coronary thrombosis in pigs, suggesting a key driver of reperfusion injury and no-reflow.

Myocardial Release of Endothelin (ET) and Enhanced ETA Receptor-Mediated Coronary Vasoconstriction After Coronary Thrombosis and Thrombolysis in Pigs

Discussion

Member takes

Implication

Key Points

Cite This Study

Myocardial Release of Endothelin (ET) and Enhanced ETA Receptor-Mediated Coronary Vasoconstriction After Coronary Thrombosis and Thrombolysis in Pigs

Discussion

Member takes

Implication

Key Points

Cite This Study

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