Complement depletion with naje haje cobra venom factor limits prostaglandin release and improves visceral perfusion in porcine endotoxic shock

Mitchell P. Fink, Heidie R. Rothschild, Yamo F. Deniz, Stephen M. Cohn

Research output: Contribution to journalArticlepeer-review

18 Scopus citations

Abstract

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-PGF (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 languageEnglish (US)
Pages (from-to)1076-1085
Number of pages10
JournalJournal of Trauma - Injury, Infection and Critical Care
Volume29
Issue number8
DOIs
StatePublished - Aug 1989

ASJC Scopus subject areas

  • Surgery
  • Critical Care and Intensive Care Medicine

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