抄録
Platelet aggregation and blood coagulation originally take actions in hemostasis. However, when the damage of vascular endothelial cells occurred, these systems are activated at the vessel walls.
In inflammation, increase in vascular permeability causes extravasation of plasma protein into interstitial space, where Factor XII is considered to be activated and then plasma prekallikrein is converted to active plasma kallikrein. In fact, in rat carrageenin-induced pleurisy, plasma kallikrein-kinin system was activated only in the pleural cavity, although this system was not activated in plasma of rats with pleurisy.
The release reaction of platelet aggregation was accompanied with release of prostaglandins (PG) and thromboxane (TX). In pleural fluid, 6-keto PGE1α, PGE2, TXB2 showed their peaks successively between 1 and 7 hours after carrageenin. 6-keto PGE1α is a stable metabolite of PGI2 and might be related to vasodilatation and anti-aggregation, whereas TXB2 might be result of platelet aggregation. TXA2, however, is also released during phagocytosis and the peak of TXB2 in pleural fluid agreed with that of polymorphonuclear leucocytes in pleural fluid. The main PG responsible to exudation was PGE2. Thus, in inflammatory reactions, due to invasion of incitors, blood coagulation and thrombus formation seems to be hardly involved, unless bleeding occurred.
On the contrary, thrombus formation plays important roles in rejection of the skin graft. Blood flow to the skin graft reopened 6-9 days after implantation, but several days later, blood flow ceased suddenly by thrombus formation in arterioles and small veins at the boarder of the graft skin.
Arachidonic acid (C, 20: 4) is important as precursor of PG in platelet aggregation and in the inhibition by vascular endothelial cells. In take of fishes results in increase of eicosapentaenoic acid (C 20: 5) in phospholipids, which causes prevention of the thrombus formation.
