Complement activation by the hydroxyl radical during intestinal reperfusion. Shock 1994 Dec;2(6):445-50
Date
12/01/1994Pubmed ID
7743376DOI
10.1097/00024382-199412000-00010Scopus ID
2-s2.0-0028702973 (requires institutional sign-in at Scopus site) 37 CitationsAbstract
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.
Author List
Turnage RH, Magee JC, Guice KS, Myers SI, Oldham KTMESH terms used to index this publication - Major topics in bold
AnimalsChemotactic Factors
Complement Activation
Complement C5a
Deferoxamine
Disease Models, Animal
Hydroxyl Radical
Intestines
Male
Neutrophils
Rats
Rats, Sprague-Dawley
Reperfusion Injury
Thiourea