Complement activation by the hydroxyl radical during intestinal reperfusion

This study examines the hypothesis that hydroxyl radical (OH.) generation during intestinal reperfusion activates the complement system forming the potent chemotaxin C5a. Anesthetized Sprague-Dawley rats underwent 120 min of intestinal ischemia and 60 min of reperfusion (IIR). Complement (C) activat...

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Bibliographic Details
Published in:Shock (Augusta, Ga.) Ga.), 1994-12, Vol.2 (6), p.445-450
Main Authors: Turnage, R H, Magee, J C, Guice, K S, Myers, S I, Oldham, K T
Format: Article
Language:English
Subjects:
Animals
Chemotactic Factors - biosynthesis
Complement Activation - drug effects
Complement Activation - physiology
Complement C5a - antagonists & inhibitors
Complement C5a - biosynthesis
Deferoxamine - pharmacology
Disease Models, Animal
Hydroxyl Radical - metabolism
Intestines - blood supply
Intestines - injuries
Male
Neutrophils - physiology
Rats
Rats, Sprague-Dawley
Reperfusion Injury - immunology
Reperfusion Injury - physiopathology
Thiourea - analogs & derivatives
Thiourea - pharmacology
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Summary:This study examines the hypothesis that hydroxyl radical (OH.) generation during intestinal reperfusion activates the complement system forming the potent chemotaxin C5a. Anesthetized Sprague-Dawley rats underwent 120 min of intestinal ischemia and 60 min of reperfusion (IIR). Complement (C) activation was assessed by measuring total plasma C activity and C5a-related chemotaxis and leukoaggregation. Dimethylthiourea and the iron chelator deferoxamine were utilized to assess the role of the OH. in the activation of C in this model. Sham-operated animals served as controls. Total plasma C activity of animals sustaining IIR was 64% of controls (p < .05). Plasma of animals sustaining IIR induced greater chemotaxis and leukoaggregation than plasma from sham-operated groups (p < .05). Treatment of IIR plasma with anti-C5a antibody ameliorated the enhanced leukoaggregation characteristic of IIR plasma. Pretreatment with dimethylthiorea and deferoxamine prevented reperfusion-induced activation of complement and inhibited the chemotactic activity of plasma from IIR animals. These data are consistent with the hypothesis that IIR activates complement and that the OH. generated during reperfusion may be one mechanism by which C is activated in this injury model.
ISSN:1073-2322
DOI:10.1097/00024382-199412000-00010