The influence of blood flow on the behaviour of blood cells with particular reference to thrombosis.
Blood platelets can initiate arterial thrombosis by aggregating on atheromatous lesions and by accelerating the intrinsic coagulation system. The conversion of unreactive to reactive platelets (platelet activation) may be due to contact with vessel wall collagen and/or haemodynamic abnormalities in narrowed arteries, increasing the physical and chemical interactions with erythrocytes. Platelet activation is difficult to demonstrate and quantify in vivo. Proposed parameters include appearance of procoagulant (platelet factor 3) activity and other platelet-derived aggregating agents, notably prostaglandin endoperoxides and thromboxanes; appearance of "spontaneous" aggregates in the blood; alterations in ultrastructure, e.e., fewer dense inclusion bodies indicating the release reaction; and appearance of other released materials, e.g., platelet factor 4 which neutralises heparin and beta-thromboglobulin, both measurable by radioimmunoassay. Investigations of the biomedical mechanisms underlying platelet activation has brought up inhibitors of their reactions to aggregating agents in vitro and in vivo. Increases in bleeding time caused by such agents indicate that one or other may, if otherwise acceptable, be effective therapeutically against platelet-dependent thromboses. The recent discovery of prostacyclin and its biological effects may explain some of the problems besetting the outcome and interpretation of clinical trials so far.
D000244:Adenosine Diphosphate / Q000502:physiology; D001161:Arteriosclerosis / Q000503:physiopathology; D001773:Blood Cells / Q000502:physiology*; D003094:Collagen; D004912:Erythrocytes / Q000502:physiology; D006801:Humans; D010974:Platelet Aggregation; D012039:Regional Blood Flow; D013927:Thrombosis / Q000503:physiopathology*
D000244:Adenosine Diphosphate; D003094:Collagen