Hans Anton Lehr

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Institute of Pathology, University of Mainz, Medical Center, Mainz, Germany

Cigarette smoke contains large amounts of carcinogenic and cocarcinogenic substances that explain the increased burden of malignant tumors in smokers, particularly in the lungs, the upper gastrointestinal system, and the urinary bladder. Nonneoplastic diseases associated with cigarette smoking include chronic bronchitis and pulmonary emphysema, gastrointestinal ulcers, and a significantly increased risk of cardiovascular diseases, ranging from peripheral artery disease to myocardial infarction and cerebrovascular incidences. Although the exact pathophysiological link between cigarette smoking and cardiopulmonary disease progression remains incompletely understood, it has been recognized that a key role is played by effects on diverse aspects of the microcirculation both in terms of morphological (i.e., vessel wall injury, capillary loss) and functional aspects. The latter concerns predominantly changes in tissue perfusion and its regulatory mechanisms (i.e., reactive hyperemia, sequestration of blood cells in the microcirculation). The mechanisms of action of cigarette smoking on the microcirculation include compromised endothelium-dependent vasorelaxation, platelet aggregation, endothelial cell dysfunction, the activation of circulating leukocytes, and eventually the aggregation and adhesion of leukocytes and/or platelets to the microvascular endothelium. In the following, an effort is made to review the existing knowledge on microcirculatory dysfunction(s) induced by cigarette smoking. For references, the reader is referred to a recent review on this subject [1].

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