In hypoxia/ischaemia and ischaemia/reperfusion, human neurophils are likely to play an important role in the development of endothehal cell damage in the microcirculation. Buflomedil hypochloride improves the capillary perfusion in such related situations, evoking a possible effect upon neutrophils. Using in vitro models of cell adhesion, buflomedil decreased 100% of histamin related neutrophil adhesion (flow sytem) and partially inhibited adhesion after IL-1–4 hours (flow and stable systems). Hypoxia induced neutrophil adhesion (4 hours) was also reduced by buflomedil, which decreased the expression of P-selectin at the surface of endothehal cells. As adenosin (NECA) exhibited the same results in hypoxia and theophylline inhibited them, such results support an action of buflomedil presumably via the A2 receptor.

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