Initiation of white cell activation during cardiopulmonary bypass: cytokines and receptors

Journal of Cardiovascular Pharmacology
D Cameron

Abstract

The pathogenesis of organ injury induced by extracorporeal circulation involves many inflammatory cascades and cellular components of the immune system. One therapeutic approach is to target the neutrophil and minimize the deleterious effects of neutrophil activation during bypass. Mechanical removal of circulating neutrophils from the perfusate by filtration produced profound leukopenia in a dog model that persisted for 8-12 h post-bypass. The leukocyte-depleted animals had less lung sequestration of white cells than control animals and less evidence of white-cell activation. These differences resulted in significantly improved pulmonary gas exchange in the post-bypass period. Another approach to reducing cardiopulmonary bypass (CPB) neutrophil-mediated injury is modulation of neutrophil-endothelial adherence. One strategy is to improve the biocompatibility of the bypass circuit. Our laboratory measured the upregulation of the neutrophil-adhesion molecules CD11b and CD18 during CPB but did not demonstrate significant differences between membrane and bubble oxygenators. However, studies in pigs undergoing CPB with a standard extracorporeal circuit or a heparin-coated CPB circuit found less pulmonary injury in the heparin-coated...Continue Reading

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Citations

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