Two Mechanisms of Immunologically-Induced Injury to Rabbit Platelets

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Abstract
Summary: Platelet injury (release of platelet 5-hydroxytryptamine) that occurs when antigen and antibody are added to non-immune platelet-rich plasma has been compared and contrasted to platelet injury that occurs when preformed immune precipitates are used as the challenge. Platelet injury by large concentrations of immune precipitate is not inhibited by citrate, by anticomplementary concentrations of heparin or sodium chloride, or by prior pepsin digestion of the antibody from which the precipitates are prepared. Prior zymosan adsorption of plasma at 16°C in the presence of Na2H2EDTA inhibits the precipitate-platelet interaction. Platelet injury produced by soluble antigen and antibody in non-immune platelet-rich plasma is inhibited by citrate, by anticomplementary concentrations of heparin and sodium chloride, and by prior pepsin digestion of the antibody. Prior zymosan adsorption of plasma at 16°C in the presence of Na2H2EDTA is, however, without effect. It is postulated that platelet injury by immune precipitates in citrated plasma results from phagocytosis of the precipitates by platelets and does not require complement, that platelet injury by soluble antigen and antibody in heparinized plasma is a complement-dependent process, and that platelet injury by immune precipitates in heparinized plasma may involve both mechanisms.

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