[The effect of benzydamine on various functions of human granulocytes and their interaction with endothelial cells]

The influence of the non-steroidal antiinflammatory drug benzydamine (Tantum) was studied on several functions of human polymorphonuclear leukocytes, namely their adhesion to endothelial cells, the leukocyte auto-aggregation and their locomotion into cellulose nitrate filters or on glass surfaces. The granulocytes were stimulated either by the synthetic oligopeptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) or the physiologically important complement anaphylatoxins C3a and C5a-desArg. The experiments showed that benzydamine reduces effectively the attachment of granulocytes to endothelium of isolated guinea pig aortic strips (IC50 3-4 X 10(-6) mol/l). This effect seems to be exclusively due to the inhibition of granulocyte adhesiveness and cannot be washed out. Benzydamine also diminishes leukocyte aggregation induced by either the complement peptides C3a, C5a-desArg or FMLP, and in addition causes deaggregation of already formed leukocyte aggregates. However, benzydamine is inhibitory only at 1-3 X 10(-4) mol/l. Likewise, C5a-desArg-induced leukotaxis and phagocyte polarization on glass surfaces as well as spontaneous migration of unstimulated granulocytes in Boyden chambers are decreased only at 10(-4) mol/l. By contrast, benzydamine usually augments chemotaxis in Boyden chambers induced by concentration gradients of the stimuli. This effect might be explained by the prevention of the known auto-oxidative inhibition of phagocytes exerted by benzydamine. Regarding the therapeutic significance, inhibition of the leukocyte-endothelial interaction appears to be of considerable pharmacologic relevance to explain the antiphlogistic properties of benzydamine in vivo.