Neutrophil adhesion molecule expression during cardiopulmonary bypass with bubble and membrane oxygenators

Glucocorticoids are very effective inhibitors of both the acute and chronic inflammatory response. In this study the hypothesis that glucocorticoids inhibit an early component of the inflammatory response, neutrophil adhesion to endothelium, by down-regulation of adhesion molecules on neutrophils or endothelium was examined. No effect of dexamethasone on neutrophil adhesion to endothelium or of antigen expression by neutrophils or endothelium was found. The mechanism of action of glucocorticoids in the inflammatory response is probably not mediated by alterations in adhesion molecules.

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Neutrophil activation and adhesion molecule expression in a canine model of open heart surgery with cardiopulmonary bypass

Cardiovascular Research ◽

10.1016/s0008-6363(96)88612-3 ◽

1995 ◽

Vol 29 (6) ◽

pp. 775-781 ◽

Cited By ~ 16

Author(s):

W. J Dreyer ◽

L. H Michael ◽

E. E Millman ◽

K. L Berens

Keyword(s):

Cardiopulmonary Bypass ◽

Adhesion Molecule ◽

Heart Surgery ◽

Open Heart Surgery ◽

Canine Model ◽

Neutrophil Activation ◽

Adhesion Molecule Expression ◽

Open Heart

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Neutrophil activation and adhesion molecule expression in a canine model of open heart surgery with cardiopulmonary bypass

Cardiovascular Research ◽

10.1016/0008-6363(96)88612-3 ◽

1995 ◽

Vol 29 (6) ◽

pp. 775-781 ◽

Cited By ~ 31

Author(s):

W Dreyer

Keyword(s):

Cardiopulmonary Bypass ◽

Adhesion Molecule ◽

Heart Surgery ◽

Open Heart Surgery ◽

Canine Model ◽

Neutrophil Activation ◽

Adhesion Molecule Expression ◽

Open Heart

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rHuG-CSF Increases the Platelet-Neutrophil Complex Formation and Neutrophil Adhesion Molecule Expression in Volunteer Granulocyte and Stem Cell Apheresis Donors

Therapeutic Apheresis and Dialysis ◽

10.1111/j.1744-9987.2006.00361.x ◽

2006 ◽

Vol 10 (2) ◽

pp. 180-186 ◽

Cited By ~ 4

Author(s):

Cavidan Karadogan ◽

Ihsan Karadogan ◽

Aynur Ugur Bilgin ◽

Levent Undar

Keyword(s):

Stem Cell ◽

Complex Formation ◽

Adhesion Molecule ◽

Neutrophil Adhesion ◽

Adhesion Molecule Expression

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Neutrophil adhesion and the inflammatory response induced by cardiopulmonary bypass

Cardiology in the Young ◽

10.1017/s1047951100001633 ◽

1993 ◽

Vol 3 (3) ◽

pp. 244-250 ◽

Cited By ~ 7

Author(s):

Adam Finn ◽

William J. Dreyer

Keyword(s):

Cardiopulmonary Bypass ◽

Inflammatory Response ◽

Neutrophil Adhesion ◽

Complement Cascade ◽

Extracorporeal Circuit ◽

Secretory Function ◽

Anaphylatoxin C5a ◽

Vascular Beds ◽

Membrane Oxygenators ◽

Cellular Deformability

The activation of inflammatory systems as a consequence of cardiopulmonary bypass represents one possible means by which inj ury to tissues and associated dysfunction of organs may occur in the postoperative cardiac patient, both pediatric and adult. Kirklin and colleagues demonstrated in the early 1980's that complement activation occurs as a consequence of blood exposure to the extracorporeal circuit. Subsequent studies demonstrated this to be true in systems using both bubble and membrane oxygenators. The anaphylatoxin C5a and its metabolite C5a des arg are produced during activation of the complement cascade. They are potent stimulants which may induce activation of neutrophils. This activation may be manifested as changes in shape, decreased cellular deformability, and changes in adhesive and secretory function. Activation of neutrophils by these fragments of complement could contribute to neutrophilmediated damage to tissues by promoting retention of neutrophils in vascular beds and secretion of cytotoxic substances. Recent studies demonstrating the release of neutrophil granular enzymes into the plasma following cardiopulmonary bypass are evidence that activation of neutrophils is taking place in this setting.

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