NEUTROPHIL ADHESION MOLECULE EXPRESSION DURING CARDIOPULMONARY BYPASSWITH BUBBLE AND MEMBRANE OXYGENATORS

The neutrophil-mediated tissue injury associated with cardiopulmonary bypass (CPB) is thought to require the interaction of specific neutrop hil 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 ve rsus bubble oxygenators on the expression of neutrophil CD11b and CD18 were compared; and the plasma levels of the intercellular adhesion mo lecule-1 (cICAM-1), an inducible endothelial adhesion molecule, were m easured. In addition, the time courses of complement activation and ne utrophil granule release were measured to determine their temporal rel ationship to the expression of the neutrophil adhesion molecule. Fifte en adult patients underwent procedures requiring cardiopulmonary bypas s; hollow-fiber membrane oxygenators were used in 8 (group M) and bubb le oxygenators were used in 7 (group B). Blood samples were drawn befo re, during, and after CPB for determination of the expression of neutr ophil CD11b and CD18 (immunofluorescent flow cytometry), and the plasm a cICAM-1, elastase, lactoferrin (enzyme-linked immunoabsorbent assay) , and plasma C3a (radioimmunoassay) levels. CPB caused an immediate an d sustained increase in the neutrophil CD11b and CD18 expression in bo th 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 neu trophil adhesion molecule expression was accompanied by elevations in the plasma.elastase, lactoferrin, and C3a levels; there were no differ ences between oxygenator groups for any of these parameters. Before CP B, 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 increa se in group M patients (220.5 +/- 20.6 ng/ml). These results demonstra te that (1) CPB causes upregulation of the neutrophil adhesion molecul e subunits CD11b and CD18; (2) the bubble and membrane oxygenators use d 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.