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Coronary thrombolysis and endothelin-1 release
1Department of Cardiology, School of Medicine, Tokai University, Kanagawa, Japan.
Insights
Coronary thrombus formation does not increase endothelin-1 (ET-1). However, thrombolysis of coronary thrombus leads to increased ET-1 production, suggesting resolved thrombus stimulates ET-1 release.
Area of Science:
- Cardiovascular Research
- Endocrinology
Background:
- Endothelin-1 (ET-1) is a potent vasoconstrictor implicated in cardiovascular diseases.
- The relationship between intracoronary thrombus and ET-1 levels requires further elucidation.
Purpose of the Study:
- To investigate the association between intracoronary thrombus formation and endothelin-1 (ET-1) levels.
- To determine if thrombolysis influences ET-1 production in the coronary vasculature.
Main Methods:
- A canine model of acute myocardial infarction (MI) was established using coronary occlusive thrombus.
- Blood samples were collected from the aorta and coronary vein in dogs undergoing thrombus formation, thrombolysis, or coronary ligation/reperfusion.
- Plasma ET-1 concentrations were measured in different experimental groups.
Main Results:
- Acute MI induced by occlusive thrombus showed increased ET-1 in both aorta and coronary vein.
- During thrombolysis in Group I, ET-1 levels in the coronary vein were significantly higher than in the aorta, indicating local production.
- Non-occlusive thrombus formation (Group II) and simple ligation/reperfusion (Group III) showed minimal or no significant differences in ET-1 between aorta and coronary vein.
Conclusions:
- Intracoronary thrombus formation itself does not appear to significantly stimulate ET-1 production.
- Thrombolysis of established coronary thrombi is associated with increased coronary ET-1 production, suggesting a role for the resolving thrombus as a stimulus.
- These findings highlight a potential mechanism linking thrombolysis and subsequent ET-1 release in the coronary vasculature.
Abstract:
The relation between intracoronary thrombus and endothelin-1 (ET-1) was studied. In a canine model, acute myocardial infarction (MI) was induced by coronary occlusive thrombus produced at a mock atheromatous plaque. Blood samples were collected from the aorta (A) and coronary vein (V). Twenty-eight open-chest dogs divided into three groups were studied. Group I (n = 15): acute MI was induced by coronary occlusive thrombus, and thrombolysis was obtained by urokinase two hours after MI. Group II (n = 8): nonocclusive thrombus was produced without inducing MI. Group III (n = 5): coronary artery was ligated for two hours and reperfused by release of ligation. In Group I, ET-1 was significantly increased after MI in A and V, and ET-1 in V was significantly more elevated than in A during thrombolysis, suggesting ET-1 production in the coronary vessels by thrombolysis. In Group II, ET-1 increased slightly during thrombus formation, but there was no difference in A and V. In Group III, ET-1 was elevated significantly after MI without A and V difference. These results indicate that there is no detectable ET-1 production with coronary thrombus formation, whereas coronary ET-1 production is detected during thrombolysis, most probably because resolved thrombus releases a more potent stimulus to ET-1 production.