Thromboxane, prostacyclin, and hemodynamic events in primate endotoxin shock.
Prostaglandins participate in the pathophysiology of septic shock; however, their exact role is unclear. In this study we investigated the possibility that thromboxane and prostacyclin, the most recently discovered prostaglandins, may be related to the pulmonary arterial hypertension (thromboxane) and systemic arterial hypotension (prostacyclin) during endotoxin shock in the baboon. There are no previously reported studies in the subhuman primate. In this study ten male baboons received an LD70 dose of E. coli endotoxin. Cardiac output, mean systemic arterial pressure, pulmonary arterial pressure, blood gases, WBC and platelet counts, and prostaglandins were determined at 0, 15, 60, 120, 180, and 240 minutes. Thromboxane and prostacyclin levels were significantly (P less than 0.05) increased after the endotoxin injection. Systemic arterial PGI values increased within 15 minutes, peaked at two hours, and was directly related to the fall in systemic arterial pressure (r = 0.93). In contrast, thromboxane values peaked at 15 minutes and directly related (r = 0.90) to the rise in pulmonary artery pressure. Thromboxane and prostacyclin are significantly increased in subhuman primate endotoxin shock. The temporal relationship of thromboxane and pulmonary arterial pressure suggests that thromboxane may mediate the effects of endotoxin on the pulmonary vasculature.
D000818:Animals; D001794:Blood Pressure; D011464:Epoprostenol / Q000097:blood*; D006439:Hemodynamics; D008297:Male; D010215:Papio; D011453:Prostaglandins / Q000097:blood* / Q000502:physiology; D012772:Shock, Septic / Q000097:blood* / Q000503:physiopathology; D013931:Thromboxanes / Q000097:blood*
D011453:Prostaglandins; D013931:Thromboxanes; D011464:Epoprostenol