Endotoxic shock in the piglet: beneficial effects of prostaglandin synthesis inhibition.
In anesthetized piglets the intravenous injection of a lethal dose of endotoxin, 0.5 mg/kg, resulted in a progressively evolving deterioration of the cardiovascular system (hypotension, decrease in cardiac output), in an increase in pulmonary vascular resistance and in the death of all animals within 210 min following endotoxin administration. Endotoxin induced a significant increase in immunoreactive (i) i-6-oxo-PGF1 alpha, i-TXB2, and i-15-oxo-13,14-dihydro-PGF2 alpha levels in peripheral plasma. Pretreatment with the PG-synthesis inhibitor, flurbiprofen, abolished the profound rise in PG-levels, whereas cardiovascular performance was more sustained. The results suggest the involvement of several prostanoids during the evolution of endotoxic shock in the piglet.
D000818:Animals; D015237:Dinoprost; D011464:Epoprostenol / Q000502:physiology; D005260:Female; D005480:Flurbiprofen / Q000494:pharmacology*; D006439:Hemodynamics / Q000187:drug effects*; D011422:Propionates / Q000494:pharmacology*; D011448:Prostaglandin Antagonists / Q000494:pharmacology*; D011453:Prostaglandins / Q000502:physiology*; D011460:Prostaglandins F / Q000502:physiology; D012772:Shock, Septic / Q000503:physiopathology*; D013552:Swine; D013928:Thromboxane A2 / Q000502:physiology; D014655:Vascular Resistance / Q000187:drug effects
D011422:Propionates; D011448:Prostaglandin Antagonists; D011453:Prostaglandins; D011460:Prostaglandins F; D013928:Thromboxane A2; D005480:Flurbiprofen; D015237:Dinoprost; D011464:Epoprostenol