The Role Of Red Blood Cells In Spontaneous Aggregation Of Platelets In Whole Blood

1984 
Platelets in whole blood are surrounded by and outnumbered by red blood cells. There is considerable evidence (Hellem, 1960; Gaarder et al., 1961; Harrison and Mitchell, 1966; Born et al., 1976) that adenosine 5’-diphosphate (ADP), released from red cells, causes the activation and aggregation of blood platelets. It has also been suggested (Harrison and Mitchell, 1966; Born et al., 1976; Born, 1977) that the release of ADP from red cells is enhanced in higher shear stress flow conditions. Therefore, it is likely that the leakage of ADP from red cells in pathological conditions, such as atherosclerosis, where normal blood flow is impaired, can have an important role as a trigger mechanism in platelet thrombus formation (Gaarder et al., 1961; Harrison and Mitchell, 1966; Born et al., 1976). Chlorpromazine, a drug which can stabilise red cell membranes and protect against haemolysis (Seaman, 1972), has been shown to inhibit spontaneous platelet thrombus formation in vitro (Born et al., 1976; Born and Wehmeier, 1979). These observations have led to the suggestion (Born, 1979) that chlorpromazine and drugs with similar actions on the red blood cells may be of value in the prevention of arterial thrombosis, when it is induced by the action of high shear stresses on the red cells.
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