Rudolph Tanja K, Rudolph Volker, Baldus Stephan
University Hospital Heart Center, Department of Cardiology/Angiology, 20246 Hamburg, Germany.
Proc Am Thorac Soc. 2008 Dec 1;5(8):820-3. doi: 10.1513/pats.200807-063TH.
Smoking remains the leading cause of cardiovascular disease, accounting for almost one third of cardiac deaths in the Western industrialized countries. Atherosclerosis in general, and coronary disease in particular, is now considered an inflammatory disease. Recent research has tried to better characterize the subcellular mechanisms of smoke and nicotine on the vessel wall and circulating mediators of disease. Whereas nicotine-dependent receptor activation on endothelial cells has long been considered to elicit antiinflammatory actions, recent observations reveal that nicotine evokes close interactions between the endothelium and proinflammatory cells: namely, leukocytes. Besides monocytes and macrophages, nicotine has been shown to stimulate neutrophils, a cell species long been considered irrelevant for the progression of atherosclerotic disease. Being stimulated by nicotine, neutrophils generate reactive oxygen species and release prooxidant enzymes like myeloperoxidase, which are capable of entering the vessel wall independently. Central mechanisms by which these enzymes can modulate the structural and functional integrity of the vessel wall have been characterized and increased our understanding of neutrophil-derived changes in vascular homeostasis in response to smoking and nicotine, respectively.
吸烟仍然是心血管疾病的主要病因，在西方工业化国家，几乎三分之一的心脏死亡病例都与之相关。一般而言，动脉粥样硬化，尤其是冠状动脉疾病，如今被视为一种炎症性疾病。近期的研究试图更深入地描述烟雾和尼古丁对血管壁及疾病循环介质的亚细胞机制。长期以来，人们一直认为内皮细胞上尼古丁依赖受体的激活会引发抗炎作用，但最近的观察结果表明，尼古丁会在内皮细胞和促炎细胞（即白细胞）之间引发密切相互作用。除了单核细胞和巨噬细胞外，尼古丁还被证明会刺激中性粒细胞，而中性粒细胞长期以来一直被认为与动脉粥样硬化疾病的进展无关。在尼古丁的刺激下，中性粒细胞会产生活性氧并释放髓过氧化物酶等促氧化酶，这些酶能够独立进入血管壁。这些酶调节血管壁结构和功能完整性的核心机制已得到描述，这分别加深了我们对吸烟和尼古丁导致的中性粒细胞衍生的血管稳态变化的理解。
