Brain regulation of thrombosis and hemostasis: from theory to practice.
Brain regulation of thrombosis and hemostasis: from theory to practice.
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DOI:
10.1161/strokeaha.113.000736
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发表时间:
2013-11
期刊:
影响因子:
8.3
通讯作者:
Fisher MJ
中科院分区:
文献类型:
--
作者:
Fisher MJ
Focal changes in the presence of a systemic prothrombotic state are evident in diseases of veins, arteries, and microvessels. There seems to be a dual basis for this focality, residing in the differential expression of anticoagulant and procoagulant factors within different elements of the vascular tree, along with specific effects of different organs. 6 For example, the endothelial protein C receptor (EPCR) is expressed predominantly in large arteries and veins, whereas TFPI is principally in capillaries. 6, 7 Other endothelial-dependent anticoagulant (eg, nitric oxide) and procoagulant (von Willebrand factor) molecules show predilection for arteries and veins, respectively. 6, 8Arterial thromboses are particularly dependent on loss of vascular integrity with consequent exposure of subendothelial surfaces to blood. 6 Nevertheless, thrombotic occlusion of the coronary arteries does not substantially increase with deficiencies of the protein C, protein S, or antithrombin III pathway. 5 On the contrary, deficiencies of these same factors clearly predispose to venous thrombosis. 5, 6 These venous thromboses tend to occur in the lower extremities, at sites of venous valve pockets where stagnation of flow and local hypoxia are common. 6, 9 A vastly different distribution of thrombosis occurs in the presence of polycythemia vera, paroxysmal nocturnal hemoglobinuria, and essential thrombocythemia, in which