动脉再狭窄的炎症机制  

Inflammatory Mechanism of Arterial Restenosis

作　　者：高登元[1] 董万利[1] 

机构地区：[1]苏州大学附属第一医院神经内科,215006

出　　处：《国外医学（脑血管疾病分册）》2004年第5期334-336,共3页Foreign Medical Sciences Cerebrovascular Diseases

摘　　要：动脉再狭窄的病理生理学变化涉及血管平滑肌细胞早期直接受损 ,血管内皮细胞增生 ,继而血管平滑肌细胞增殖 ,细胞外基质沉积。越来越多的证据表明 ,炎症反应在血管损伤早期血管内膜增生和血管重塑中起关键作用。普遍采用的血管支架因可引起强烈而持久的炎症反应而改变了血管对损伤的反应。白细胞聚集和浸润的细胞学和分子生物学机制已经阐明 ,这为再狭窄的治疗提供了依据。The pathophysiology of arterial restenosis involves early and direct injury to smooth muscle cells and vascular endothelial proliferation, then vascular smooth muscle proliferation and extracellular matrix deposition. More and more evidence shows that inflammatory response plays a pivotal role in the early stage of vascular injury in vascular endothelial proliferation and vascular remodeling. The widespread use of arterial stents has fundamentally altered the vascular response to injury by causing intense and prolonged inflammatory response. The mechanism of cytology and molecular biology of leukocyte recruitment and infiltration have been elucidated, this will provide the basis for the treatment of restenosis.

关 键 词：动脉再狭窄 炎症 治疗 分子生物学 白细胞聚集 白细胞浸润 

分 类 号：R543[医药卫生—心血管疾病]