The effect of nicotine on aortic endothelium (original) (raw)
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Effects of chronic oral consumption of nicotine on the rabbit aortic endothelium
The American journal of pathology, 1981
New Zealand white rabbits (10) were administered daily doses of nicotine (2.4 mg/kg/day) in their drinking water for 25 weeks. Nicotine-treated rabbits were compared with control rabbits (10) in terms of blood serum biochemistry and lipid profiles, blood cells counts, changes in aortic endothelial cell morphologic characteristic and distribution, and vessel wall permeability (Evans blue dye uptake). Fasting serum levels of glucose, triglycerides, total cholesterol, and LDL-cholesterol were elevated in nicotine-treated rabbits. No significant differences (nicotine vs control) were seen in leukocyte, erythrocyte and platelet counts, or hematocrit and hemoglobin. Control and nicotine-treated rabbit aortas showed similar focal areas of increased Evans blue dye uptake; staining was localized primarily to aortic arch areas. Endothelial cells (luminal surface) from non-Evans blue and Evans blue arch areas were examined by a combination of Häutchen preparation (silver-stained vessels) and s...
Current Vascular Pharmacology, 2007
Smoking is a significant independent risk factor for cardiovascular disease and is a leading cause of structural and functional alterations of the cardiovascular system. Most clinical and experimental investigations of the pathophysiology of cigarette smoking have studied the effects of smoke as a whole, while a few studies focused on specific components of cigarette smoke, e.g. nicotine and carbon monoxide, which are only 2 of the more than 4,000 different chemicals present in cigarette smoke. The findings point to some discrepancies when the effects of whole smoke are compared to nicotine alone, while there is almost uniform agreement that both active and passive smoking have detrimental effects on the cardiovascular system, although a milder effect was suggested for the latter.
Contribution of nicotine to acute endothelial dysfunction in long-term smokers
Journal of the American College of Cardiology, 2002
The aim of this study was to determine whether nicotine, a constituent of cigarette smoke, contributes to acute endothelial dysfunction after smoking one cigarette. BACKGROUND Animal studies suggest that nicotine might cause an impairment of endothelium-dependent vasodilation via an increase in oxidative stress.
Morphological Alterations of the Heart and Blood Vessels from Tobacco Smoke: the Steps of the Damage
Journal of Cardiology and Therapy
Two cardiovascular structures are usually involved in the harm caused by cigarette smoke: myocardium and endothelium, which are mainly affected by carbon monoxide and nicotine. The harmful effects of smoking induce functional responses that eventually lead to morphological damage. With regard to the myocardium, three main steps have been well documented: myocardial alterations related to the hypoxia caused by increased concentrations in carboxyhemoglobin, reversible degenerative alterations of the cardiac muscle and irreversible myocardial necrosis. A typical experimental pattern due to smoking effects is the smoke cardiomyopathy. Endothelial dysfunction triggers a large number of responses, mainly consisting of blood and inflammatory cell migration and adhesion at the site of altered arterial wall,rupture of the muscular and elastic cells of the arterial wall and lipid infiltrates, which lead to atherosclerosis plaque. In addition, arteriosclerosis is the result of smoking on the resistance arteries. Evidence indicates that morphological alterations of the heart and blood vessels from smoking follow a well-defined way that allow us to tell the story of the cardiovascular alterations.
Endothelial disruptive pro-inflammatory effects of nicotine and e-cigarette vapor exposures
American Journal of Physiology - Lung Cellular and Molecular Physiology, 2015
The increased use of inhaled nicotine via e-cigarettes has unknown risks to lung health. Having previously shown that cigarette smoke (CS) extract disrupts the lung microvasculature barrier function by endothelial cell activation and cytoskeletal rearrangement, we investigated the contribution of nicotine in CS or e-cigarettes (e-Cig) to lung endothelial injury. Primary lung microvascular endothelial cells were exposed to nicotine, e-Cig solution, or condensed e-Cig vapor (1–20 mM nicotine) or to nicotine-free CS extract or e-Cig solutions. Compared with nicotine-containing extract, nicotine free-CS extract (10–20%) caused significantly less endothelial permeability as measured with electric cell-substrate impedance sensing. Nicotine exposures triggered dose-dependent loss of endothelial barrier in cultured cell monolayers and rapidly increased lung inflammation and oxidative stress in mice. The endothelial barrier disruptive effects were associated with increased intracellular cera...
Endothelial Dysfunction in Passive Smokers
Journal of Cardiology & Current Research, 2014
Nowadays, there is no doubt that exposure to passive smoking, whatever it may be approached to be studied-and there are a lot of study approaches: clinical, biological, metabolic, epidemiologic, statistic and so on, that recognize different pathogenetic mechanisms of damage-leads to only one final result that is a reversibly functional harm of the heart and blood vessels following acute exposure, and pathologic alterations that become, in the long run, irreversible lesions of the above target organs after chronic exposure. The harm of the heart and blood vessels from passive smoking is the result of either an isolated action or combined action of some toxics contaminated indoor air by tobacco products, primarily nicotine and carbon monoxide. Among the different types of vessel damage caused by acute exposure to passive smoking, there is evidence that endothelial dysfunction, characterized by impaired endothelium-dependent vasodilation as a result of reduced nitric oxide (NO) production, is the earlier alteration to appear, although, initially, is transient but repeatable.