Morphological Aspects of Cigarette Smoke Induced Microvascular Dysfunction

Histomorphological studies have demonstrated thickening of the walls of pulmonary arterioles, as well as arterioles in trachea, esophagus, stomach, pancreas, and kidneys in smokers, depending on the length and severity of the smoking habit. Subsequent investigations have shown fibrous thickening in coronary and intramyocardial arterioles in smokers and in beagle dogs trained to smoke. Another organ that has been subject to intensive interest in this context is the placenta: Attempting to explain the reduced birth weight of children born to smoking mothers and the increased perinatal morbidity and mortality associated with maternal smoking, several authors have studied the placentas of smoking versus nonsmoking mothers. Smoking-related findings included a significantly reduced surface area of the fetal microvasculature, degeneration of villous capillary endothelial cells, subendothelial edema formation, and— eventually—increased syncytiotrophoblastic necrosis in placentas of smoking mothers. More recently, Lova and co-workers have demonstrated microvascular remodeling in the labial mucosa of smokers, revealing increased numbers of dystrophic capillary loops, exhibiting smaller calibers, increased tortuosity, and increased frequencies of microa-neurysms [2].

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