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


CONCLUSIONS
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.
Chan
R K
RK
Department of Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. hhechtman@partners.org
Ibrahim
S I
SI
Verna
N
N
Carroll
M
M
Moore
F D
FD
Hechtman
H B
HB
D000936:Antigen-Antibody Complex / Q000276:immunology*; D002986:Clinical Trials as Topic; D003169:Complement Inactivator Proteins / Q000627:therapeutic use; D003165:Complement System Proteins / Q000276:immunology*; D006801:Humans; D007075:Immunoglobulin M / Q000276:immunology; D008407:Mast Cells / Q000276:immunology; D017382:Reactive Oxygen Species / Q000276:immunology; D015427:Reperfusion Injury / Q000188:drug therapy / Q000276:immunology*; D013373:Substance P / Q000276:immunology
D000936:Antigen-Antibody Complex; D003169:Complement Inactivator Proteins; D007075:Immunoglobulin M; D017382:Reactive Oxygen Species; D013373:Substance P; D003165:Complement System Proteins