Prostacyclin biosynthesis and hypotension in relation to complement activation in rabbit endotoxic shock.
Intravenous endotoxin injection in rabbits led to complement activation, a biphasic hypotension and elevated arterial levels of prostacyclin and/or 6-oxo-prostaglandin F1 alpha. Primary hypotension and stimulation of prostacyclin biosynthesis were completely dependent on complement activation whereas the secondary changes of these parameters were partly complement dependent, as indicated by experiments with cobra venom factor pretreated rabbits. Prostacyclin, which was never detectable in arterial blood, contributed to the development of hypotension in rabbit endotoxic shock.
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D000818:Animals; D001794:Blood Pressure; D003167:Complement Activation; D011464:Epoprostenol / Q000096:biosynthesis*; D007022:Hypotension / Q000209:etiology / Q000503:physiopathology*; D011817:Rabbits; D012772:Shock, Septic / Q000503:physiopathology*
D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol