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The addition of latex particles to native (no anticoagulant) or citratcd human platclctrich plasma (PRP), or to a once-washed platelct suspension causes platelet aggregation. This aggregation is associated with phagocytosis of t'ae latex particles by the platelets and appcars to be due to release of adenosine diphosphate (ADP) from the platclets. Adenosinc and adenosine monophosphate, which are known to inhibit platelet aggregation induced by ADP, also block that induced by latex. These compounds do not prevent the phagocytosis of latex particles by the platelet. The addition of iodoacctate and 2,4-dinitrophcnol in appropriate concentrations to the PRP, prior to the addition of the latex, blocks platelet aggregation and phagocytosis. This is also true for the chelating agent ethylenediaminetetraacetate (EDTA). Platclets left in contact with latex for a sufficient period of time show loss of their granules. Leucocytcs phagocytose both latex and platelets that had themselves phagocytosed latex. It is concluded that phagocytosis of latex particlcs by platelcts rcscmblcs that by white cells, and that in both processes metabolic changes appear to bc involved.

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