We tested the hypothesis that complement (C′)-dependent release of prostaglandin (PG) I2 is an important factor contributing to the development of hypotension and low systemic vascular resistance index (SVRI) in endotoxic shock. Two groups (n = 7) of pentobarbital-anesthetized pigs (12–15 kg) were infused over 40 min with Escherichia coli lipopolysaccharide (LPS; 200 μg/kg) and continuously resuscitated with normal saline (1 ml/kg min): LPS-Control (no pretreatment) and LPS-Decomplemented (pretreatment 18 hr before study with 500–1, 500 units of Naje haje cobra venom factor, CVF). Prior treatment with CVF: i) decreased the mean titer of total hemolytic C′ to 15.9% of pretreatment levels; ii) significantly decreased post-LPS plasma concentrations of immunoreactive TxB2 (TxA2 metabolite) and 6-keto-PGF1α (PGI2 metabolite); iii) abrogated the early transient decrease in cardiac index observed in the LPS-Control group; iv) tended to improve post-LPS visceral perfusion assessed using radioactive microspheres; and v) had no discernible effect on the late sustained decrease in SVRI observed following infusion of LPS. We conclude that C′ activation is a major determinant of LPS-induced prostanoid release in vivo, although our results do not support the view that C′-dependent release of PGI2 is an important factor contributing to low SVRI in resuscitated endotoxic shock.
|Original language||English (US)|
|Number of pages||10|
|Journal||Journal of Trauma - Injury, Infection and Critical Care|
|State||Published - Aug 1989|
ASJC Scopus subject areas
- Critical Care and Intensive Care Medicine