Ischaemia-reperfusion is an event triggered by immune complexes and complement

Abstract

Background: Reperfusion injury is a common clinical problem that lacks effective therapy. Two decades of research implicating oxygen free radicals and neutrophils has not led to a single successful clinical trial.

Methods: The aim was to review new clinical and preclinical data pertaining to the alleviation of reperfusion injury. A review of the literature was undertaken by searching the MEDLINE database for the period 1966-2003 without language restrictions.

Results and conclusion: Evidence now points to complement and immune complexes as critical players in mediating reperfusion injury. Ischaemia is postulated to induce a phenotypical cellular change through the surface expression of a neoantigen. Preformed circulating natural IgM antibodies are then trapped and complement is activated. Final events leading to reperfusion injury include formation of the membrane attack complex and mast cell degranulation.