European Journal of Cardio-Thoracic Surgery, Vol 10, 279-283, Copyright © 1996 by European Association for Cardio-thoracic Surgery
Patterns of changes in neutrophil adhesion molecules during normothermic cardiopulmonary bypass. A clinical study
F Le Deist, P Menasche, A Bel, J Lariviere, A Piwnica and G Bloch
INSERM U-132, Hopital Necker-Enfants Malades, Paris, France.
The adhesion of activated neutrophils to endothelial cells is a key feature
of the inflammatory response to cardiopulmonary bypass (CPB) because it
"unlocks" a cascade of cytotoxic events. This adhesion is made possibly by
the sequential involvement of two sets of neutrophil cell surface
receptors: L-selection and beta 2 integrins (CD 11 a/CD 18; CD 11 b/CD 18;
CD 11 c/CD 18). We have assessed the changes in the expression of these
adhesion molecules in ten patients who underwent various open-heart
procedures with the use of "warm" (33.4 degrees-37 degrees C) CPB. Arterial
blood samples were obtained before, during and after bypass and processed
for immunofluorescent flow cytometric analysis. CD 11 a expression remained
unchanged throughout the study period. Conversely, CD 11 b drastically
increased early after the onset of bypass (at 15 min on bypass: 172 +/- 17
[mean fluorescence (arbitrary units), mean +/- SEM] versus 63 +/- 13 before
bypass. P < 0.02) and was still markedly elevated 30 min after the end
of bypass (160 +/- 38, P < 0.05 versus the pre-by-pass value). CD 11 c
expression underwent a similar upregulation (at 15 min of bypass: 54 +/- 5
versus 34 +/- 5 at baseline, P < 0.01). L-selectin expression did not
change significantly during the period of observation. Put together, these
results suggest that CPB is associated with an increased adhesive potential
of neutrophils, which enhances their binding to the vascular endothelium
and thereby initiates tissue damage through the release of cytotoxic
mediators from adherent cells. Manipulation of integrin expression could
therefore represent an effective means of alleviating the component of
bypass-induced inflammatory tissue damage which is more specifically
neutrophil-mediated.
