Pathophysiology of thromboembolism and its modulation by low-molecular-weight heparins.
Vessel wall damage and changes in hemostatic mechanisms are important factors in thrombogenesis. Vascular damage may be encountered in trauma, inflammatory processes, and other forms of vascular disease. Systemic changes in platelets and in certain coagulation constituents also contribute to thrombus formation. The generation of thrombin seems to be a pivotal event in thrombogenesis, and inactivation of this enzyme has been attempted for many years with heparin, low-molecular-weight heparin, and other glycosaminoglycans. Different forms of heparin may act differently, and the future must more clearly elucidate the role of the endothelium in all of these processes.
Breddin
H K
HK
International Institute of Thrombosis and Vascular Diseases, Frankfurt am Main, Germany.
D000818:Animals; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D006495:Heparin, Low-Molecular-Weight / Q000494:pharmacology* / Q000627:therapeutic use; D006801:Humans; D051381:Rats; D013917:Thrombin / Q000096:biosynthesis; D013923:Thromboembolism / Q000188:drug therapy / Q000503:physiopathology*
D006495:Heparin, Low-Molecular-Weight; D013917:Thrombin