Reperfusion injury of ischemic skeletal muscle is mediated by natural antibody and complement. Academic Article uri icon

Overview

abstract

  • Reperfusion of ischemic tissue induces an acute inflammatory response that can result in necrosis and irreversible cell injury to both local vascular endothelium and parenchyma. To examine the pathogenesis of ischemia/reperfusion injury, we have used mice deficient in complement components C3, C4, or serum immunoglobulin in a hindlimb model of ischemia. We found that mice homozygous deficient in C3 or C4 were equally protected against reperfusion injury based on a significant reduction in leakage of radiolabeled albumin out of the vasculature. This demonstrates that classical pathway complement is an important factor in the initiation of inflammation following reperfusion. Furthermore, mice deficient in serum immunoglobulin were equally protected and this protection could be reversed by reconstitution with serum from normal mice. Thus, this report describes a novel mechanism for reperfusion injury that involves antibody deposition and activation of complement leading to inflammation permeability.

publication date

  • May 1, 1996

Research

keywords

  • Complement System Proteins
  • Immunoglobulins
  • Ischemia
  • Muscle, Skeletal
  • Reperfusion Injury

Identity

PubMed Central ID

  • PMC2192547

Scopus Document Identifier

  • 0030014528

Digital Object Identifier (DOI)

  • 10.1084/jem.183.5.2343

PubMed ID

  • 8642343

Additional Document Info

volume

  • 183

issue

  • 5