Release of prostaglandin F2alpha during splanchnic artery occlusion shock.
Prostaglandin F2alpha concentrations were determined in hepatic portal venous plasma of dogs during splanchnic artery occlusion (SAO) shock and in nonshock control dogs. Dogs subjected to SAO shock exhibited a dramatic decrease in mean arterial blood pressure and significant increases in portal venous PGF2alpha and amino-nitrogen concentrations, as well as in cathepsin D and MDF activities. Dogs treated with indomethacin prior to SAO shock did not exhibit a significant increase in portal venous PGF2alpha. Indomethacin had no effect on the increase of plasma amino-nitrogen and only slightly reduced portal venous cathepsin D activity during SAO shock. Nevertheless, indomethacin significantly attenuated the severity of the postrelease hypotension observed in SAO shock and diminished the plasma accumulation of MDF. These studies indicate that prostaglandins are released from the splanchnic region during SAO shock and that this release can be prevented by pretreatment with indomethacin. The role of endogenously released prostaglandins in SAO shock is not clear, but the magnitude of the increase warrants further study.
D000818:Animals; D001798:Blood Proteins; D002403:Cathepsins / Q000097:blood; D004285:Dogs; D007213:Indomethacin / Q000494:pharmacology; D007511:Ischemia; D008026:Ligation; D008297:Male; D008638:Mesenteric Arteries; D009201:Myocardial Depressant Factor / Q000097:blood; D009584:Nitrogen / Q000097:blood; D011458:Prostaglandins E / Q000097:blood*; D011460:Prostaglandins F / Q000276:immunology; D011863:Radioimmunoassay; D012769:Shock / Q000097:blood*
D001798:Blood Proteins; D009201:Myocardial Depressant Factor; D011458:Prostaglandins E; D011460:Prostaglandins F; D002403:Cathepsins; D009584:Nitrogen; D007213:Indomethacin