Platelets and leucocytes release a number of substances that can activate or inhibit other circulating cells, and may reciprocally interact to form mixed aggregates. Stimulated leucocytes may release strong platelet agonists (1-3) or inhibitors of platelet aggregation (4-7), thus making the study of their interaction with platelets a very exciting and puzzling subject. When a turbidimetric technique is used to evaluate leucocyte/ platelet interaction in vitro, the change in optical density may be due to a change in the number of either cell type. This may not be relevant in the presence of maximal aggregation, but it limits evaluation of threshold changes in platelet activation. We recently observed that stimulation of human platelet-rich plasma or washed platelet suspensions with low concentrations of aggregating agents induced a change in shape or limited reversible aggregation, as measured by optical density; but reduced platelet count up to 10% -15% , as evaluated by a platelet analyzer (Baker 810 Instrument; A. De Mori, Milan, Italy). Using the latter method, we studied human platelet response to a stable analogue of endoperoxide (U46619) in the presence of autologous polymorphonuclear leucocytes (PMN). U46619 was used in two dosage ranges: 60-150 nmol/1, which induced only shape change; and 210-450 nmol/1, which induced irreversible aggregation, as measured by optical aggregometer. Platelet shape
[1]
G. Bazzoni,et al.
Inhibition of platelet function by polymorphonuclear leukocytes.
,
1990,
The Journal of laboratory and clinical medicine.
[2]
Z. M. Chen,et al.
Platelet activation by polymorphonuclear leukocytes exposed to chemotactic agents.
,
1990,
The American journal of physiology.
[3]
J. Vane,et al.
Human neutrophils and mononuclear cells inhibit platelet aggregation by releasing a nitric oxide-like factor.
,
1989,
Proceedings of the National Academy of Sciences of the United States of America.
[4]
S. Moncada,et al.
Synthesis of nitric oxide from L-arginine by neutrophils. Release and interaction with superoxide anion.
,
1989,
The Biochemical journal.
[5]
M. Chignard,et al.
Cathepsin G is a strong platelet agonist released by neutrophils.
,
1988,
The Biochemical journal.
[6]
M. Chignard,et al.
Direct evidence for the existence of a neutrophil-derived platelet activator (neutrophilin).
,
1986,
Proceedings of the National Academy of Sciences of the United States of America.
[7]
G. de Gaetano,et al.
Human blood leucocytes in vitro generate an inhibitor of platelet aggregation.
,
1981,
Thrombosis research.