Rabbit lung macrophages stimulate platelets in vitro as observed by density-gradient centrifugation and transmission electron microscopy

Abstract

Both platelets and macrophages play a role in the pathogenesis of atherosclerosis. To examine whether they may interact and, if they do, to elucidate the mechanisms of such an interaction, suspensions of the two cell types from rabbits were mixed together, then subjected to Stractan density-gradient centrifugation and transmission electron microscopy. Suspensions of only one cell type served as controls. When otherwise unstimulated platelets and macrophages came into contact with each other, the platelets became less dense. Ultrastructurally, the platelets underwent shape changes without losing their granules, and were often arranged around the macrophages like a rosette. The processes of the macrophages became elongated. ADP caused a similar shift in platelet density and, when the cell types were together, increased this shift. With ADP the rosetting was abolished, but platelet aggregates were found to be in superficial contact with the macrophages. With thrombin the contact between the platelet aggregates and macrophages was close. Addition of platelet antagonists showed that the shift in platelet density and the rosetting upon contact with macrophages are dependent on divalent cations. Neither ADP, nor thrombin, nor PAF seem to be involved in the reactions.

Modulation of Blood Cell Activation by Four Commonly Used Anticoagulants

“…EDTA tended also to suppress platelet degranulation in whole blood (Fig. 5), which is confirmed by a study of Jgrgensen et al (31) who showed that rosetting of platelets upon contact with macrophages is dependent on divalent cations and therefore inhibited by EDTA.…”