[Organic nitrates and prostaglandins in the cardiovascular system]

The beneficial effect of organic nitrates in acute myocardial ischemia is commonly explained by their hemodynamic actions, especially the dilatation of venous capacitance vessels. Recent studies have shown an inhibition of platelet function by organic nitrates ex vivo but not in vitro. Antiplatelet activities of organic nitrates might represent an additional mechanism, independent of vascular actions which might eventually involve stimulation of prostacyclin formation by the vessel wall. In vitro experiments on isolated coronary artery preparations have demonstrated stimulation of PGI2 as well as inhibition of platelet thromboxane synthesis by a number of organic nitrates. Optimal stimulation requires the presence of a free nitro group in the molecule at a particular steric position and can be suppressed by a number of inhibitors, including corticosteroids, indomethacin and methylene blue. Administration of the organic nitrate teopranitol to healthy volunteers is associated with depressed platelet secretion ex vivo which is not seen with the compound in vitro. It is concluded that further clinical elucidation of the PGI2-related mechanism in the action of organic nitrates in patients appears to be both necessary and useful.