Abstract

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-PGF 1α, i-TXB 2, and i-15-oxo-13,14-dihydro-PGF 2α 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.

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