Influence of heparin, aspirin, streptokinase and factor VIII (AHF) on amorphous electron-dense substance, a mediator of platelet and thrombus adhesion in vivo.
Platelet adherence and aggregation on vessel walls are the first crucial steps in thrombogenesis and atherosclerosis. Whether platelets can be activated on damaged endothelial cells or their activation is achieved only when subendothelial structures are exposed was controversially discussed in the past. Recently, an electron-microscopic study has revealed an amorphous electron-dense substance (AEDS) after endothelial cell damage and has discussed its role as a possible trigger of thrombogenesis. The aim of the present study is to elucidate the role and origin of this substance and to investigate the influence which inhibitors of platelet function (acetylsalicylic acid), coagulation (heparin), stimulation of fibrinolysis (streptokinase) and addition of factor VIII (AHF) have on AEDS.
D000268:Adhesiveness; D000818:Animals; D001241:Aspirin / Q000494:pharmacology*; D001777:Blood Coagulation; D001792:Blood Platelets / Q000378:metabolism*; D006224:Cricetinae; D004727:Endothelium / Q000378:metabolism; D005169:Factor VIII / Q000494:pharmacology*; D006493:Heparin / Q000494:pharmacology*; D008647:Mesocricetus; D010973:Platelet Adhesiveness; D013300:Streptokinase / Q000494:pharmacology*
D005169:Factor VIII; D006493:Heparin; D013300:Streptokinase; D001241:Aspirin