Exposure to passive smoking: A test to predict endothelial dysfunction and atherosclerotic lesions
Exposure to passive smoking: A test to predict endothelial dysfunction and atherosclerotic lesions
复制标题
DOI：
10.1177/0003319707306300
复制
发表时间：
2008-04-01
期刊：
影响因子：
2.8
通讯作者：
Balbarini, Alberto
中科院分区：
文献类型：
--
作者：
Leone, Aurelio;Balbarini, Alberto
急性暴露于环境烟草烟雾（ETS）被认为是不利影响动脉粥样硬化。本文的目的是评估ETS暴露后内皮功能障碍受试者的肱动脉超声检查是否与动脉粥样硬化病变相关。研究了从不吸烟的健康志愿者（n = 18）和既往心肌梗死（MI; n = 10）受试者。健康志愿者为12名男性（66%）和6名女性（34%），平均年龄为34 - 9岁。MI后受试者为平均年龄为53.8 ± 4.8岁的男性。在静息状态下评估内皮功能（通过肱动脉超声检查）后，研究受试者接受了两次肱动脉超声检查：在无烟环境中，然后在被香烟燃烧污染的相同环境中（35 ppm一氧化碳浓度）。碳氧血红蛋白浓度测定前和后ETS暴露。基线肱动脉直径，反应性充血时的直径，舌下含服硝酸甘油（GTN）（内皮非依赖性血管扩张剂）后的直径分别在休息时和无烟及吸烟环境下测量。每例研究受试者作为其自身对照。两组之间没有进行比较。在两组中均观察到ETS暴露与内皮功能障碍之间的强相关性。MI后受试者还显示内皮非依赖性血管舒张恶化，这通常是由于动脉壁改变。ETS暴露后，GTN后平均血流介导的血管舒张功能仅在MI后受试者中显著降低（P <0.01）。两组的碳氧血红蛋白浓度均升高（P <0.01）。ETS暴露可能是一种有效的测试，以确定内皮功能障碍和动脉壁的改变，通过使用肱动脉超声。
Acute exposure to environmental tobacco smoke (ETS) is considered to adversely influence atherogenesis. The aim of this article was to assess whether brachial ultrasonography in subjects with endothelial dysfunction after ETS exposure is associated with atherosclerotic lesions. Never smoker healthy volunteers (n = 18) and subjects with a previous myocardial infarction (MI; n = 10) were studied. Healthy volunteers were 12 men (66%) and 6 women (34%) with a mean age of 34 9 years. Post-MI subjects were men with a mean age of 53.8 +/- 4.8 years. After assessing endothelial function (by brachial ultrasonography) at rest, study subjects underwent brachial ultrasonography twice: in a smoke-free environment and then in the same environment polluted by cigarette combustion (35 ppm carbon monoxide concentration). Carboxyhemoglobin concentration was measured before and after ETS exposure. Baseline brachial-artery diameter, diameter during reactive hyperemia, and diameter after sublingual nitroglycerin (GTN) administration (endothelium-independent vasodilator) were measured at rest and in both smoke-free and smoking environments. Each study subject acted as their own control. No comparison was made between the two groups. A strong correlation between ETS exposure and endothelial dysfunction was observed in both groups. Post-MI subjects also showed endothelium-independent vasodilation worsening, which is usually due to arterial wall alterations. After ETS exposure, mean flow-mediated vasodilation after GTN was significantly (P < .01) reduced only in post-MI subjects (P < .01). Carboxyhemoglobin concentration increased in both groups (P < .01). ETS exposure may be an effective test to identify endothelial dysfunction and arterial wall alterations by using brachial ultrasonography.