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 109E. 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 > 80% of pre-bacteremic levels. In Groups I, II, and III, cardiac output fell to < 50% of baseline within 1 hr and remained there throughout the study. FP in Groups I and II rose to > 200% of baseline (P<.02 and <.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 pre-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.
|Number of pages||5|
|State||Published - Jan 1 1988|