[Hemodynamic effects of nitroglycerin following acute inhibition of prostaglandin synthesis].
The mechanism of action by which nitrates produce vasodilation has not been fully clarified so far. Experimental studies indicate a possible relationship to the prostaglandin system. This study describes the consequences of acute prostaglandin synthesis inhibition on the hemodynamic effects of nitroglycerin in patients with stable angina pectoris. Intravenous application of 1 g acetylsalicylic acid was associated with a small but significant blunting of the pressure decline in the pulmonary and systemic circulation following the sublingual administration of 0.8 mg nitroglycerin. Premedication with 75 mg indomethacin i.m. was followed by a decrease in pressure decline in the pulmonary artery during intravenous nitroglycerin infusion. Significant inhibition of prostaglandin synthesis was shown by a substantial decline in plasma levels of circulating prostaglandin metabolites in both experiments. These results indicate that the mechanism of action of nitroglycerin may be partially mediated by vasodilatory prostaglandins.
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000328:Adult; D000787:Angina Pectoris / Q000188:drug therapy*; D001241:Aspirin / Q000627:therapeutic use*; D016861:Cyclooxygenase Inhibitors; D015232:Dinoprostone; D011464:Epoprostenol / Q000097:blood; D005080:Exercise Test; D005260:Female; D006439:Hemodynamics / Q000187:drug effects*; D006801:Humans; D007213:Indomethacin / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D005996:Nitroglycerin / Q000627:therapeutic use*; D011453:Prostaglandins / Q000097:blood*; D011458:Prostaglandins E / Q000097:blood
D016861:Cyclooxygenase Inhibitors; D011453:Prostaglandins; D011458:Prostaglandins E; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; D005996:Nitroglycerin; D015232:Dinoprostone; D001241:Aspirin; D007213:Indomethacin
Hämodynamische Wirkungen von Nitroglycerin nach akuter Hemmung der Prostaglandinsynthese.