Functional Aspects of Cigarette Smoke Induced Microvascular Dysfunction

In terms of functional effects of the cigarette smoke impaired microvasculature, the accessibility of the skin microcirculation to noninvasive diagnostic techniques (i.e., plethysmography, nailfold microscopy, laser Doppler fluxmetry) has resulted in an abundant literature on the effect of cigarette smoking on skin perfusion in humans and experimental animals. These studies have found that baseline blood flow in the skin of smokers is reduced either permanently and/or after smoking one or more cigarettes. Also, reactive hyperemia is compromised in the skin of neonatal infants born to smoking mothers and in the skin of adult smokers—in terms of both peak blood flow and recovery time. The study by Asano and Branemark is of particular interest to microcirculation researchers because of its unique experimental approach: These authors implanted titanium observation chambers into the upper arm skin of human volunteers and recorded by intravital microscopy the micro-circulatory flow velocity during cigarette smoke exposure [3]. Similar results have later been reproduced using intravital microscopy on the nailfold capillary bed, the labial mucosa, and the retina of smoking human subjects. Intravital microscopic studies have found that chronic exposure of rats and pigs to tobacco smoke or to oral nicotine significantly reduces red blood cell velocity and blood flow through capillaries of the mesentery, the intervertebral disc, and the testis. The situation has been found more complex for cigarette smoke effects on the cerebrovascular microcirculation. Whereas several studies have demonstrated reductions in cerebral blood flow in chronic smokers, acute cigarette smoke exposure has resulted in contradictory results in both animals and humans, with some authors reporting increases and some decreases in cerebral blood flow.

oxygen-dependent mechanisms and where NO inactivation prevented subsequent acetylcholine-induced vasodilation. A similar reduction of basal NO activity has later been reported in coronary and brachial arteries of chronic smokers, and recent evidence suggests that cigarette smoke extract decreases the inducible form of NO synthase in an endothelial cell culture and that NO synthase is reduced in saphe-nous vein grafts explanted from chronic smokers. Several experimental and clinical observations have focused on the oxidative stress hypothesis, suggesting that reactive oxygen species either contained in cigarette smoke or released from smoke-activated neutrophils may contribute the endothelial dysfunction.

Intravital microscopy on the hamster cheek pouch model found that topical superfusion with cigarette smoke extract attenuates acetylcholine-induced dilation of resistance arte-rioles and that application of superoxide dismutase effectively restored endothelium-dependent arteriolar dilation after nicotine superfusion, suggesting a key role of reactive oxygen species in the induction of endothelial dysfunction. Similar results have been obtained with aqueous extracts of smokeless tobacco and the studies were later extended to the effect of cigarette smoke extract and/or nicotine on other important cellular vasodilator pathways, including adeny-late cyclase and ATP-sensitive potassium channels.

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