Endotoxin-induced prostaglandin E and F release in dogs.
Prostaglandin E and F (PGE and PGF) levels in sequential blood samples obtained simultaneously from the renal and portal veins and aorta during endotoxin shock in dogs were determined by radioimmunoassay. Four groups of dogs were studied. In five control dogs in which no endotoxin was given, PGE and PGF levels did not change significantly at 0, 15, 30, 60, and 90 min. In eight dogs given endotoxin alone, PGE and PGF levels did not change in the aorta. In samples taken from the portal vein there was a significant rise in PGE and PGF 15 min after endotoxin, whereas renal vein PGE and PGF did not become significantly elevated until 60 and 90 min after endotoxin. In six dogs pretreated with acetylsalicylic acid and six dogs pretreated with indomethacin, PGE and PGF levels did not change after endotoxin. Indomethacin modified the delayed hemodynamic effects of endotoxin whereas acetylsalicylic acid did not. Neither drug blocked the immediate hemodynamic effects of endotoxin. Endotoxin-induced PGE and PGF release is probably due to increased synthesis. The mechanism whereby synthesis is stimulated and the extent to which vasomotor tone is influenced by PGE and PGF during endotoxin shock cannot be determined from our data.
D000818:Animals; D001011:Aorta; D001241:Aspirin / Q000494:pharmacology; D001794:Blood Pressure; D002302:Cardiac Output; D004285:Dogs; D007213:Indomethacin / Q000494:pharmacology; D011169:Portal Vein; D011453:Prostaglandins / Q000097:blood*; D012082:Renal Veins; D012772:Shock, Septic / Q000097:blood*; D013997:Time Factors; D014690:Venous Pressure
D011453:Prostaglandins; D001241:Aspirin; D007213:Indomethacin