[The effect of decomplementation on model experimental inflammatory responses (rat paw oedema) (author's transl)]

An investigation was carried out of the effect of decomplementation by either aggregated human gamma globulin (aggHGG) -- activating the classical complement cascade -- or cobra-venom factor (CVF) -- acting through the alternative pathway -- on rat paw oedema induced by various agents. The direct, passive Arthus reaction (DPA) and dextran-and carrageenin-induced oedema were inhibited by both decomplementing measures, whilst serotonin-and formalin-induced oedema remained unaffected. The paw swelling induced by synthetic bradykinin was significantly reduced only by aggHGG, not by CVF. These observations strongly support -- but do not yet prove -- the assumption that complement is involved in the development not only of the DPA but also of the responses to the polysaccharides, dextran and carrageenin in the rat. The partial inhibition of bradykinin-induced paw oedema by aggHGG and not by CVF might be explained by a densensitization or blocking of bradykinin receptors by a peptide derived from the early-reacting complement components (C 1, 4, 2). Investigations of the effect of aggHGG and CVF on blood pressure, haematocrit, partial thromboplastin time, plasmakininogen and kinase activity, leucocytes and thrombocytes indicate that non-complement-dependent factors are unlikely to be involved in the observed inhibition of experimental rat paw oedema.