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Ann Thorac Surg 1993;56:847-853
© 1993 The Society of Thoracic Surgeons
Department of Cardiac Surgery and Division of Immunology, Department of Pediatrics, The Johns Hopkins Medical Institutions, and Scios Nova Inc, Baltimore, Maryland USA
* Address reprint requests to Dr Cameron, Department of Cardiac Surgery, The Johns Hopkins Hospital, 600 N Wolfe St, Blalock 618, Baltimore, MD 21287.
The neutrophil-mediated tissue injury associated with cardiopulmonary bypass (CPB) is thought to require the interaction of specific neutrophil and endothelial adhesion molecules. In this study, the effects of CPB on the expression of neutrophil CD11b and CD18 (the components of the Mac-1 adhesion molecule) were examined; the effects of membrane versus bubble oxygenators on the expression of neutrophil CD11b and CD18 were compared; and the plasma levels of the intercellular adhesion molecule-1 (cICAM-1), an inducible endothelial adhesion molecule, were measured. In addition, the time courses of complement activation and neutrophil granule release were measured to determine their temporal relationship to the expression of the neutrophil adhesion molecule. Fifteen adult patients underwent procedures requiring cardiopulmonary bypass; hollow-fiber membrane oxygenators were used in 8 (group M) and bubble oxygenators were used in 7 (group B). Blood samples were drawn before, during, and after CPB for determination of the expression of neutrophil CD11b and CD18 (immunofluorescent flow cytometry), and the plasma cICAM-1, elastase, lactoferrin (enzyme-linked immunoabsorbent assay), and plasma C3a (radioimmunoassay) levels. CPB caused an immediate and sustained increase in the neutrophil CD11b and CD18 expression in both groups; after 60 minutes of CPB, CD11b expression had increased by 116.9% ± 19.1% in group B and by 79.3% ± 8.5% in group M (p = 0.78). Over the same period, CD18 expression increased by 97.2% ± 17.9% in group B and by 72.4% ± 16.8% in group M (p = 0.67). Increased neutrophil adhesion molecule expression was accompanied by elevations in the plasma elastase, lactoferrin, and C3a levels; there were no differences between oxygenator groups for any of these parameters. Before CPB, the plasma cICAM-1 levels were similar in the two groups (group B, 175.6 ± 25.6 ng/ml; group M, 200.2 ± 30 ng/ml). Twenty-four hours after CPB, the plasma cICAM-1 level increased to 289.1 ± 31.1 ng/ml in group B patients (p < 0.004 versus the baseline) but did not increase in group M patients (220.5 ± 20.6 ng/ml). These results demonstrate that (1) CPB causes upregulation of the neutrophil adhesion molecule subunits CD11b and CD18; (2) the bubble and membrane oxygenators used in this study cause similar degrees of neutrophil adhesion molecule upregulation, neutrophil degranulation, and complement activation; and (3) use of bubble, but not membrane, oxygenators results in increased plasma cICAM-1 levels.
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