Endothelial dysfunction, impaired endogenous fibrinolysis, and cigarette smoking - A mechanism for arterial thrombosis and myocardial infarction
Endothelial dysfunction, impaired endogenous fibrinolysis, and cigarette smoking - A mechanism for arterial thrombosis and myocardial infarction
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DOI：
10.1161/01.cir.99.11.1411
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发表时间：
1999-03-23
期刊：
影响因子：
37.8
通讯作者：
Webb, DJ
中科院分区：
文献类型：
--
作者：
Newby, DE;Wright, RA;Webb, DJ
背景-有效的内源性纤溶需要从血管内皮细胞快速释放组织纤溶酶原激活物(TPA)。吸烟是动脉血栓形成和心肌梗死的已知危险因素，并会导致内皮功能障碍。因此，我们研究了吸烟对人体体内P物质诱导的tPA释放的影响。方法和结果-测量了12名吸烟者和12名年龄和性别匹配的非吸烟者的双前臂血流和血浆纤溶因子，这些人接受了单侧臂动脉注射P物质(2~8pmol/min)。在吸烟者和非吸烟者中，P物质引起血流量和血浆tPA抗原和活性的局部释放呈剂量依赖性增加(P
Background-Effective endogenous fibrinolysis requires rapid release of tissue plasminogen activator (tPA) from the vascular endothelium. Smoking is a known risk factor for arterial thrombosis and myocardial infarction, and it causes endothelial dysfunction. We therefore examined the effects of cigarette smoking on substance P-induced tPA release in vivo in humans.Methods and Results-Blood flow and plasma fibrinolytic factors were measured in both forearms of 12 smokers and 12 age- and sex-matched nonsmokers who received unilateral brachial artery infusions of substance P (2 to 8 pmol/min). In both smokers and nonsmokers, substance P caused dose-dependent increases in blood flow and local release of plasma tPA antigen and activity (P