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Oxygen free radical activity during live E. coli septic shock in the dog. Circ Shock 1988 Aug;25(4):319-23 PMID: 3048773

Pubmed ID

3048773

Abstract

Free radicals generated during purine catabolism or by activated granulocytes cause tissue injury by peroxidation of lipid membranes. In a canine model of sepsis initiated by intravenous live Escherichia coli, fluorescent products of lipid peroxidation (FP) were measured in serum. Four groups of five dogs infused with 10(9)E. coli/kg were analyzed--I: no further treatment; II: prior depletion of granulocytes with a cytotoxic antibody; III: pre-treatment with superoxide dismutase and catalase; and IV: resuscitation after bacterial infusion to maintain cardiac output greater than 80% of pre-bacteremic levels. In Groups I, II, and III, cardiac output fell to less than 50% of baseline within 1 hr and remained there throughout the study. FP in Groups I and II rose to greater than 200% of baseline (P less than .02 and less than .03). In Groups III and IV, FP did not rise significantly from baseline. The rise in serum FP and the prevention of this rise by-treatment with antioxidants indicate generation of oxygen radicals. Their presence had no effect on hemodynamic parameters. Granulocyte depletion did not alter appearance of FP; however, prevention of low cardiac output blocked FP formation. These data suggest that oxygen free radicals were generated by tissue ischemia, rather than by granulocytes, in this model of septic shock.

Author List

Morgan RA, Manning PB, Coran AG, Drongowski RA, Till GO, Ward PD, Oldham KT

Author

Keith T. Oldham MD Professor in the Surgery department at Medical College of Wisconsin




Scopus

2-s2.0-0023732970   17 Citations

MESH terms used to index this publication - Major topics in bold

Animals
Cardiac Output
Catalase
Dogs
Escherichia coli Infections
Free Radicals
Granulocytes
Lipid Peroxidation
Oxygen
Shock, Septic
Spectrometry, Fluorescence
Superoxide Dismutase
jenkins-FCD Prod-310 bff9d975ec7f2d302586822146c2801dd4449aad