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Coronary vasodilation by nitrates is not mediated by the prostaglandin system: a quantitative cineangiographic study
Insights
Prostaglandins do not mediate large coronary artery vasodilation from nitrates. Aspirin did not affect nitrate-induced vasodilation, and nitrate-induced vasodilation was not affected by prostaglandins.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Nitroglycerin and related nitrates are potent vasodilators used in treating cardiovascular conditions.
- Prostaglandins are implicated in regulating vascular tone and mediating vasodilation.
- The specific role of prostaglandins in nitrate-induced coronary vasodilation requires clarification.
Purpose of the Study:
- To investigate the role of prostaglandins in mediating vasodilation of large coronary arteries induced by nitrates.
- To assess the effect of aspirin on nitrate-induced coronary vasodilation.
- To determine if prostaglandins influence resting coronary artery tone.
Main Methods:
- Quantitative magnification coronary angiography was used to measure coronary artery diameter changes.
- Aspirin (systemic and intracoronary) was administered to patients.
- Intracoronary isosorbide dinitrate was given to induce vasodilation.
- Urinary 6-ketoprostaglandin-F1 alpha levels were measured to assess prostacyclin excretion.
Main Results:
- Intracoronary isosorbide dinitrate significantly increased coronary diameter both before and after aspirin administration.
- Aspirin did not alter the vasodilatory response to isosorbide dinitrate.
- Aspirin did not affect resting coronary artery tone.
- Urinary prostacyclin excretion was significantly reduced after the study procedures.
Conclusions:
- Prostaglandins do not play a role in mediating the vasodilation of large coronary arteries by nitrates.
- Nitrate-induced coronary vasodilation is independent of prostaglandin activity.
- The study findings rule out a significant role for prostaglandins in modulating coronary vascular tone at rest.
Abstract:
The possible role of prostaglandins in mediating large coronary artery vasodilation by nitrates was investigated by quantitative magnification coronary angiography. The effects of aspirin (1 g systemically and 100 mg intracoronary) in preventing large coronary artery vasodilation induced by intracoronary isosorbide dinitrate was investigated in 16 patients. Of these, 5 received 0.3 mg (Group 1A) and 11 received 3 mg (Group 1B) intracoronary isosorbide dinitrate, before and 15 minutes after aspirin. Relative to control, 0.3 mg isosorbide dinitrate induced a 19 +/- 9% (mean +/- SD) (p less than 0.01) and 19.5 +/- 11% (p less than 0.01) increase in coronary diameter before and after aspirin, respectively (p = NS). Changes after 3 mg isosorbide were 23 +/- 12% (p less than 0.01) and 26.5 +/- 14% (p less than 0.01), respectively, before and after aspirin (p = NS). In 10 additional patients (Group 2), the effect of the same dose of aspirin on rest coronary artery tone was assessed: changes relative to control were 0.9 +/- 5.5% (p = NS) minutes after aspirin. The intracoronary administration of 3 mg isosorbide dinitrate produced a 24.7 +/- 11% increase in coronary diameter (p = NS versus pre- and postaspirin isosorbide in Group 1B). Urinary 6-ketoprostaglandin-F1 alpha values in urine samples collected in the 8 hours before and the 8 hours after the study in five patients in Group 1B and five patients of Group 2, revealed a 36 +/- 14% (mean +/- SD) reduction in excretion of prostacyclin (p less than 0.01). These data rule out a role for prostaglandins both in mediating dilation of large coronary arteries by nitrates and in affecting their vascular tone at rest.