Humoral and cellular activation in a simulated extracorporeal circuit.
Endothelial injury consequent upon widespread humoral and cellular activation is probably a major contributor to the phenomenon of cardiopulmonary bypass-induced organ dysfunction. This article reviews some of the mechanisms by which complement and neutrophil activation and interleukin-8 may be involved in this inflammatory response. In a model consisting of a simulated extracorporeal circulation we were able to demonstrate complement activation, profound and specific changes in neutrophil adhesion molecule expression, and interleukin-8 generation. The importance of these changes and their potential interactions are discussed.
Moat
N E
NE
Royal Brompton National Heart and Lung Hospital, London, England.
Rebuck
N
N
Shore
D F
DF
Evans
T W
TW
Finn
A H
AH
D000917:Antibody Formation / Q000502:physiology*; D002315:Cardiopulmonary Bypass / Q000009:adverse effects; D002448:Cell Adhesion / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000097:blood; D003167:Complement Activation / Q000502:physiology; D005112:Extracorporeal Circulation; D006801:Humans; D007111:Immunity, Cellular / Q000502:physiology*; D016209:Interleukin-8 / Q000502:physiology; D019041:L-Selectin; D008213:Lymphocyte Activation / Q000502:physiology; D008955:Models, Cardiovascular; D009504:Neutrophils / Q000502:physiology; D012016:Reference Values
D015815:Cell Adhesion Molecules; D016209:Interleukin-8; D019041:L-Selectin