抄録
There exist several theories on pathogenesis of arteriosclerosis, in which thrombogenic theory has been one of the main ones.
In thrombogenic theory, platelet would play an important role both in blood stream and in blood vessel walls. It is commonly recognized that platelet itself does not adhere or aggregate in contact with intact vessel walls, e.g. intact endothelial lines. From the standpoint that platelet aggregation is caused either by the endothelial damages or by hyperaggregability due to chemical or hormonal stimulants, we were going to detect wether the platelet aggregation was induced by chemical or hormonal agents, and wether the endothelial cell is exfoliated even from the intact vessel walls.
(Results and Discussion)
1) Arachidomic acid induced platelet aggregation in vitro, which was inhibited by PGE1 and PGE2.
2) 1-methionine and 1-homocysteine induced platelet aggregation, which was inhibited by pyridoxal-phosphate.
3) Polysaccharides such as D-glucosamine, D-galactosamine and DEAE-dextran, accelerated the platelet aggregation induced by ADP, noradrenaline and collagen.
4) Polypeptides such as polylysine, protamine and fibrinogen induced platelet aggregation.
5) We could find the relatively large, flat, and enucleated cells (about 25μm×25μm) in the circulating blood. Although the cell itself might be deprived from venous vessel walls, several reports emphasized that this would correspond to the endothelial cells in arterial vessel walls.
From these findings, we would suppose that the endothelial cells are always exfoliated from vessel walls, and that the chemical or hormonal stimulants to platelets may always irrigate platelet function, which would cause platelet aggregation even in normal vessel walls. The homeostasis between vessel walls and platelet sensibility to stimulants might be the most important factor for preventing arteriosclerosis.
