POTENTIATION BY RED-BLOOD-CELLS OF SHEAR-INDUCED PLATELET-AGGREGATION - RELATIVE IMPORTANCE OF CHEMICAL AND PHYSICAL-MECHANISMS
- 1 January 1984
- journal article
- research article
- Vol. 64 (6) , 1200-1206
Abstract
Red blood cells (RBC) may potentiate platelet adherence and platelet aggregation (PAG) in different flow systems in vitro as well as hemostatic platelet plug formation in response to vascular injury. RBC apparently enhance PAG induced by well-defined, low-intensity, uniform, laminar shear stress. Potentiation by [human] RBC of shear-induced PAG was associated with appreciable loss of adenine nucleotides from 14C-adenine-labeled RBC, the extent of which increased with increasing RBC concentration. The concentrations of RBC-derived ADP measured in the medium after shear, as determined by both high pressure liquid chromatography and the luciferin/luciferase system, were within the range of concentrations of ADP which may trigger PAG or potentiate PAG induced by low concentrations of other platelet agonists in the aggregometer. To assess the relative contribution of chemical (ADP) and physical (platelet surface transport) mechanisms in the RBC-mediated potentiation of shear-induced PAG, aliquots of citrated platelet-rich plasma (C-PRP) were exposed to shear stress in the presence of untreated RBC or RBC exposed to an antihemolytic concentration (5 .mu.mol/l) or the membrane stabilizing agent, chlorpromazine (CPZ). Potentiation of shear-indcuced PAG in the RBC-CPZ system was significantly less than that in the untreated RBC system. CPZ-induced reduction of PAG potentiation was associated with an increase rather than a decrease in loss of adenine nucleotides from RBC. Shear-induced PAG in C-PRP as well as ADP- and collagen-induced PAG in C-PRP in the aggregometer was significantly inhibited by 5 .mu.mol/l CPZ, indicating that the observed reduced potentiation of shear-induced PAG by RBC in the presence of CPZ was due to a direct inhibitory effect of the drug on platelets rather than a reduction or shear-induced liberation of ADP from RBC. When aliquots of C-PRP were exposed to shear stress in the presence of RBC completely depleted of ADP by fixation in 1% glutaraldehyde, potentiation of PAG was .apprx. 1/2 of that observed with intact RBC. Both RBC-derived ADP and RBC-mediated platelet surface transport apparently are involved in the potentiation by RBC of PAG induced by laminar shear stress.This publication has 13 references indexed in Scilit:
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