An assessment of the participatory role of prostaglandins and serotonin in the pathophysiology of endotoxic shock.
The well-documented acute cardiodynamic changes in canine endotoxemia were significantly altered by pretreatment with either a newly synthesized serotonin receptor antagonist (ketanserin) or with a prostaglandin synthetase inhibitor (indomethacin). Ketanserin, but not indomethacin, significantly attenuated the endotoxin-induced pulmonary hypertension and vasoconstriction but had no effect on the typical systemic hemodynamic changes. In sharp contrast, indomethacin significantly attenuated systemic hypotension and enhanced peripheral vascular resistance. Neither drug influenced the typical acute fall in cardiac output or the capillary permeability edema; neither drug attenuated the metabolic acidosis of endotoxemia. These results imply that, although serotonin and the prostaglandins each participate in a unique manner in the pathophysiology of experimentally induced endotoxic shock, neither autacoid appeared singularly responsible for the hemodynamic and metabolic alterations consistently observed.
D000818:Animals; D004285:Dogs; D006439:Hemodynamics / Q000187:drug effects; D007213:Indomethacin / Q000494:pharmacology*; D007650:Ketanserin; D010100:Oxygen / Q000097:blood; D010880:Piperidines / Q000494:pharmacology*; D011453:Prostaglandins / Q000502:physiology; D011652:Pulmonary Circulation; D012701:Serotonin / Q000502:physiology; D012702:Serotonin Antagonists / Q000494:pharmacology*; D012772:Shock, Septic / Q000209:etiology* / Q000503:physiopathology
D010880:Piperidines; D011453:Prostaglandins; D012702:Serotonin Antagonists; D012701:Serotonin; D007650:Ketanserin; D010100:Oxygen; D007213:Indomethacin