title: Blood constitution: platelet aggregation, bleeding, and involvement of leukocytes.
abstract: Normally functioning endothelial cells prevent exposure of the circulating blood to thrombogenic components of the subendothelial matrix. When the vascular endothelium is injured or denuded, blood cell components are attracted to the vessel wall, where they aggregate. Endothelial damage anywhere in the body can induce hypercoagulability and contribute to the onset of brain and myocardial infarction. The components of Virchow's Triad--blood flow conditions, blood components, and vascular walls--all contribute to the formation of pathological thrombi. Improving any one component results in reduction in the rate of thrombotic disease by directly and indirectly improving the function of other contributors. Evidence supports the effectiveness of antiplatelet and anticoagulant therapy in the prevention of brain and myocardial infarction.
authors.affiliation: Department of Medicine, Tokai University School of Medicine, Institute of Medical Science, Tokai University, Isehara, Kanagawa, Japan.
authors.forename: Shinya
authors.initials: S
authors.lastname: Goto
mesh_terms: D000818:Animals; D001783:Blood Flow Velocity / Q000502:physiology; D020520:Brain Infarction / Q000097:blood* / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000293:injuries / Q000503:physiopathology*; D005343:Fibrinolytic Agents / Q000627:therapeutic use; D006470:Hemorrhage / Q000503:physiopathology*; D006801:Humans; D007511:Ischemia / Q000517:prevention & control; D007962:Leukocytes / Q000502:physiology; D009203:Myocardial Infarction / Q000097:blood / Q000503:physiopathology; D010974:Platelet Aggregation / Q000502:physiology*
chemical_list: D005343:Fibrinolytic Agents