Gairola C G, Drawdy M L, Block A E, Daugherty A
Graduate Center for Toxicology, College of Pharmacy, 229 THRI Bldg., University of Kentucky, Lexington, KY 40546-0236, USA.
Atherosclerosis. 2001 May;156(1):49-55. doi: 10.1016/s0021-9150(00)00621-3.
Epidemiological studies have strongly implicated active and passive smoking with increased risk of cardiovascular diseases. The present study was performed to determine if exposure to sidestream cigarette smoke (SSCS), a surrogate of environmental tobacco smoke, promotes atherogenesis in a mouse model of human atherosclerosis. Female ApoE-deficient mice, maintained on a Western diet, were exposed to SSCS in a whole-body exposure chamber for a total of 6 h each day, 5 days a week for 7, 10 and 14 weeks. Animals exposed to filtered ambient air served as controls. Elevated concentrations of blood carboxyhemoglobin and pulmonary CYP1A1 ascertained effective exposure of animals to SSCS. There were no consistent changes in serum concentrations of cholesterol between control and SSCS-exposed mice. Morphometric assessment of grossly discernible lesions covering the intimal area of aorta showed remarkable increases in SSCS-exposed mice at all three exposure durations studied. Increases in the lesion area defined by en face measurements were accompanied by parallel increases in the levels of esterified and unesterified cholesterol in the aortic tissues of SSCS mice. These results clearly demonstrate promotion of atherosclerotic lesion development by tobacco smoke in an atherosclerosis-susceptible mouse model.
流行病学研究有力地表明，主动吸烟和被动吸烟会增加患心血管疾病的风险。本研究旨在确定接触侧流香烟烟雾（SSCS，环境烟草烟雾的替代物）是否会在人类动脉粥样硬化小鼠模型中促进动脉粥样硬化的发生。将维持西式饮食的雌性载脂蛋白E缺乏小鼠，每周5天，每天在全身暴露舱中暴露于SSCS 6小时，持续7、10和14周。暴露于过滤后的环境空气中的动物作为对照。血液中碳氧血红蛋白浓度升高和肺部CYP1A1水平升高确定动物有效暴露于SSCS。对照小鼠和暴露于SSCS的小鼠之间血清胆固醇浓度没有一致变化。对主动脉内膜区域明显可见病变的形态学评估显示，在所研究的所有三个暴露时间段，暴露于SSCS的小鼠病变均显著增加。通过正面测量定义的病变面积增加伴随着SSCS小鼠主动脉组织中酯化胆固醇和未酯化胆固醇水平的平行增加。这些结果清楚地证明了在动脉粥样硬化易感小鼠模型中，烟草烟雾促进了动脉粥样硬化病变的发展。
