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Coronary vasodilation by nitrates is not mediated by the prostaglandin system: an angiographic and hemodynamic study
Insights
Nitrates do not rely on prostaglandins for coronary vasodilation. Aspirin (ASA) did not affect nitrate-induced vasodilation, indicating prostaglandins are not involved in this process.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Nitrates are commonly used to treat angina.
- The mechanism of nitrate-induced vasodilation is not fully understood.
- Prostaglandins are known mediators of vasodilation.
Purpose of the Study:
- To investigate the potential role of prostaglandins in mediating coronary vasodilation induced by nitrates.
- To determine if aspirin (ASA), an inhibitor of prostaglandin synthesis, affects nitrate-induced vasodilation.
Main Methods:
- 13 patients were studied.
- Coronary artery diameter was measured using quantitative magnification coronary angiography.
- Coronary sinus flow was assessed using coronary sinus thermodilution.
- Patients received isosorbide dinitrate (ISDN) and aspirin (ASA) via intracoronary and intravenous routes.
Main Results:
- Aspirin did not induce significant changes in coronary artery diameter.
- Aspirin did not prevent isosorbide dinitrate-induced vasodilation.
- Aspirin did not alter the relative vasodilation induced by isosorbide dinitrate at the coronary resistance level.
Conclusions:
- Coronary vasodilation induced by nitrates is not mediated by the prostaglandin system.
- These findings suggest an alternative pathway for nitrate action in the coronary arteries.
Abstract:
The possible role of prostaglandins in mediating coronary vasodilation by nitrates was investigated in 13 patients. In nine patients (Group 1), the effects of ISDN on coronary-artery diameter and (in four of the nine) coronary sinus flow before and after administration of ASA were compared. In four additional patients (Group 2) the first ISDN administration was omitted in order to investigate the effect of ASA on resting coronary artery tone. Dosages used were 3 mg intracoronary ISDN and 1.0 g intravenous and 100 mg intracoronary ASA. Coronary artery diameter was analyzed by means of quantitative magnification coronary angiography. Coronary sinus flow was investigated by means of coronary sinus thermodilution. ASA was not able to induce significant changes in coronary artery diameter when injected before administration of ISDN or to prevent ISDN-induced vasodilation. At the coronary resistance level, ASA was not able to prevent the relative vasodilation induced by ISDN. It is concluded that coronary vasodilation by nitrates is not mediated by the prostaglandin system.
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