TOBACCO SMOKE COMPONENTS AND ATHEROSCLEROSIS

吸烟是导致癌症发生的主要因素。 心血管疾病，包括动脉粥样硬化。它还诱导了一种 高度复杂的药理作用，主要是因为每个吸烟者 每一次用烟雾气溶胶吸入超过3800种化合物 天。其中几种化合物被认为与加速 动脉粥样硬化形成，但到目前为止，疾病的演示类似于 人类对个体烟雾的反应尚未在动物身上得到证实 成分，或吸入的总烟雾。 这项提议的目的是发起这样的调查并 识别烟草烟雾中可能具有致动脉粥样硬化作用的部分 在动脉壁上。我们将扩展和描述我们的初步 中国人动脉粥样硬化发展的观察(包括本文) 叙利亚金黄仓鼠暴露在主流烟雾中18个月。 具体地说，通过组织学、形态学和生化方法， 我们建议分析来自对照组和动物的主动脉组织。 暴露在烟雾组分以及总主流烟雾中，以及 根据个别风险确定斑块形成的程度 吸烟的因素。动脉粥样硬化的增加 在人体吸烟者的尸检中展示，但分配给 只有通过动物生物测定才能确定相对风险，因为动物生物测定具有因果关系 关系是可以测试的。 我们将在叙利亚金黄仓鼠中进行研究，这是一个久负盛名的 烟雾暴露的动物模型。他们对吸烟制度是宽容的， 循环中的血脂水平与人类相似，并对 烟草特有的致癌物质。另外，我们的初步结果， 证明这些动物会产生生化标记 长期暴露在主流香烟烟雾中的动脉粥样硬化。 香烟烟雾中具有致动脉粥样硬化作用的组份 仍有待阐明。考虑到正在更换的香烟 产品，这项研究是必不可少的确定相对风险 不同的卷烟产量和开发减少 心血管风险。

Cigarette smoking is a major contributing factor for the development of cardiovascular diseased including atherosclerosis. It induces also a hightly complex pharmacological action, primarily because each smoker inhales with the smoke aerosol more than 3,800 compounds many times each day. Several of these compounds have been associated with accelerated atherogenesis, but as yet, demonstration of disease similar to that seen in humans has not been verified in animals in response to individual smoke constitutents, or to the total inhaled smoke. It is the aim of this proposal to initiate such an investigation and to identify fractions of tobacco smoke which might exert atherogenic effects on the arterial wall. We will extend and characterize our preliminary observations (included herein) on the development of atherosclerosis in Syrian golden hamsters exposed to mainstream smoke for 18 months. Specifically, through histological, morphological and biochemical methods, we proposed to analyze aortic tissue derived from controls and from animals exposed to smoke fractions, as well as total mainstream smoke, and to determine the extent of plaque formation in response to the isolated risk factor of cigarette smoking. Increased atheroscherosis has been demonstrated at autopsy in human cigarette smokers, but assignment of relative risk can be made only with animal bioassays where cause and effect relationships can be tested. We will conduct our studies in Syrian golden hamsters, a well established animal model for smoke exposure. They are tolerant of the smoking regimes, have circulating lipid levels similar to humans and respond to tobacco-specific carcinogens. In addition, our preliminary results demonstrate that these animals develop biochemical markers of atherosclerosis during long-term exposure to mainstream cigarette smoke. The fractions present in cigarette smoke which exert atherogenic effects remain to be elucidated. With consideration of the changing cigarette product, this research is essential in determining relative risks of various cigarette yields and for developing concepts for reducing cardiovascular risks.