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Inhibition of neutrophil L-selectin shedding: a potential anti-inflammatory effect of aprotinin

British Heart Foundation Cardiac, Surgery Unit, National Heart and Lung Institute, Imperial College School of Medicine at Hammersmith Hospital, London

Kenneth M Taylor

British Heart Foundation Cardiac, Surgery Unit, National Heart and Lung Institute, Imperial College School of Medicine at Hammersmith Hospital, London

Dorian O Haskard

British Heart Foundation Cardiovascular Medicine Unit, National Heart and Lung Institute, Imperial College School of Medicine at Hammersmith Hospital, London, UK

R Clive Landis

British Heart Foundation Cardiovascular Medicine Unit, National Heart and Lung Institute, Imperial College School of Medicine at Hammersmith Hospital, London, UK, r.landis{at}ic.ac.uk

The cardiopulmonary bypass (CPB)-related inflammatory response involves leucocyte activation and increased leucocyte-endothelial cell interaction. L-selectin is an adhesion molecule expressed on the surface of leucocytes which participates in the initial rolling step of the leucocyte-endothelial cell adhesion cascade. L-selectin is proteolytically cleaved off the surface of leucocytes when they become activated, an event that is regarded as a marker of leucocyte activation. Aprotinin is a protease inhibitor that has been used in cardiac surgery as a haemostatic agent and also exhibits certain anti-inflammatory properties. In this study, peripheral venous blood from volunteers was pre-incubated with aprotinin at 200, 800 and 1600 kallikrein inhibiting units (kiu)/ml and stimulated with the chemoattractants N-formyl-methyl-leucyl-phenylalanine (fMLP) or platelet activating factor (PAF). Surface expression of L-selectin on neutrophils was measured using a monoclonal antibody and flow cytometry. The results demonstrate that aprotinin inhibits shedding of L-selectin in a dose-dependent fashion (p=0.0278 and 0.0005, respectively, at 800 and 1600 kiu/ml for fMLP-stimulated shedding; p=0.0017 and 0.0010, respectively, at 200 and 800 kiu/ml for PAF-stimulated shedding). This effect may be of significance with respect to the anti-inflammatory action of aprotinin in patients undergoing CPB.

Perfusion, Vol. 15, No. 6, 495-499 (2000)
DOI: 10.1177/026765910001500604


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