Role of platelets and thrombosis in mechanisms of acute occlusion and restenosis after angioplasty.
Role of platelets and thrombosis in mechanisms of acute occlusion and restenosis after angioplasty.
复制标题
血小板和血栓形成在血管成形术后急性闭塞和再狭窄机制中的作用。
DOI：
10.1016/0002-9149(87)90479-6
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Harker,LA
中科院分区：
文献类型：
--
作者：
Harker,LA
由血管成形术产生的血管破裂通过血小板粘附和循环血小板的募集过程引发血小板沉积以形成扩大的附壁血小板血栓。通过内皮下结缔组织结构同时激活凝血级联反应产生的凝血酶可增强血小板沉积，并稳定与纤维蛋白缠结形成的血栓。血小板募集涉及纤维蛋白原和其它细胞粘附蛋白（包括纤连蛋白、血小板反应蛋白和血管性血友病因子）的糖蛋白II B III a a受体的表达。血管成形术引起的血小板沉积和血栓形成似乎在2种并发症的发生中起重要作用：急性血栓性闭塞和再狭窄。实验性机械性血管损伤产生了可预测的，虽然相当可变的，由于短暂的平滑肌细胞增殖性初始病变形成的血管狭窄量。这种由增殖的平滑肌细胞引起的内膜增厚部分由血小板有丝分裂原介导，特别是血小板衍生生长因子，其在血管成形术时从血小板释放到受损血管中。血小板衍生生长因子也可能在机械损伤后从其他相关血管和血细胞释放，例如内皮细胞、单核细胞/巨噬细胞和平滑肌细胞本身。治疗性血管成形术后介导再狭窄的实际有丝分裂原及其来源细胞仍有待确定。在许多对照临床试验中，各种口服抗血小板药物已被证明可减少动脉血栓闭塞，例如，阿司匹林用于短暂性脑缺血发作和不稳定型心绞痛，阿司匹林和潘生丁用于隐静脉冠状动脉搭桥术和外周血管疾病的进展，潘生丁用于人工心脏瓣膜。急性动脉血栓形成可能需要更有效、立即和短暂的干预，例如抗血小板受体表达的单克隆抗体。使用各种抗血小板方案的适当对照试验适用于血管成形术患者，以评价其预防再狭窄的能力。
The vascular disruption produced by angioplasty initiates platelet deposition through the processes of platelet adhesion and recruitment of circulating platelets to form an enlarging mural platelet thrombus. Thrombin produced by simultaneous activation of the coagulation cascade by subendothelial connective tissue structures enhances platelet deposition and stabilizes the forming thrombus with enmeshing fibrin. Platelet recruitment involves the expression of the glycoprotein II b III a a receptor for fibrinogen and other cytoadhesive proteins including fibronectin, thrombospondin and von Willebrand factor. Platelet deposition and thrombus formation caused by angioplasty appear to be important in the development of 2 complications: acute thrombotic occlusion and restenosis. Experimental mechanical vascular injury produces a predictable, although rather variable, amount of vascular narrowing due to transient smooth muscle cell proliferative initimal lesion formation. This intimal thickening by proliferating smooth muscle cells is in part mediated by platelet mitogens, particularly platelet-derived growth factor, which are released into the damaged vessel from platelets at the time of angioplasty. Platelet-derived growth factor may also be released from other associated vascular and blood cells in response to mechanical injury, eg, endothelium, monocyte/macrophage and smooth muscle cells themselves. The actual mitogens, and their cells of origin, that mediate restenosis after therapeutic angioplasty remain to be established. Various oral antiplatelet agents have been shown to reduce arterial thrombotic occlusion in a number of controlled clinical trials, eg, aspirin in transient ischemic attacks and unstable angina, aspirin and dipyridamole in saphenous vein coronary artery bypass and progression of peripheral vascular disease and dipyridamole in artificial heart valves. Acute arterial thrombosis may require more potent, immediate and transient intervention, eg, monoclonal antibody to platelet receptor expression. Properly controlled trials using various antiplatelet regimens are indicated in angioplasty patients to evaluate their capacity to prevent restenosis.
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--
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期刊：
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