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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cigarette smoking is associated with an increased risk and extent of advanced atherosclerotic vascular disease in peripheral as well as coronary arteries. The likelihood of claudication, amputation, stroke, abdominal aortic aneurysm, and failure of vascular reconstruction is higher in smokers than nonsmokers. Smoking exerts its deleterious effects through many interactive mechanisms. Nicotine and carbon monoxide produce acute cardiovascular consequences, including altered myocardial performance, tachycardia, hypertension, and vasoconstriction. Smoking injures blood vessel walls by damaging endothelial cells, thus increasing permeability to lipids and other blood components. Among metabolic and biochemical changes induced by smoking are elevated plasma, free fatty acids, elevated vasopressin, and a thrombogenic balance of prostacyclin and thromboxane A2. Chronic smoking is associated with a tendency for increased serum cholesterol, reduced high density lipoprotein, and other lipid effects that contribute to atherosclerosis. In addition to rheologic and hematologic changes from increased erythrocytes, leukocytes, and fibrinogen, smokers have alterations in platelet aggregation and survival that produce thrombosis. Considering the ubiquitous repercussions of this menace, vascular surgeons should play an active role in motivating their patients to quit smoking.
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PMID:The peripheral vascular consequences of smoking. 206 25

Nicotine is the addictive substance in tobacco and its withdrawal is responsible for a range of unpleasant symptoms after smoking cessation. Although it produces acute physiological effects, nicotine alone is not carcinogenic and does not appear to cause the vascular disease associated with smoking. Nicotine replacement has been shown to be a safe and effective pharmacological treatment for tobacco dependence in certain smokers. Its efficacy is greatest when prescribed for those who are motivated and highly nicotine-dependent. It is probably not indicated for smokers with a low degree of nicotine dependence. Studies of nicotine chewing gum conducted in special referral clinics have generally produced positive results, whereas those conducted in community practice settings have shown a smaller benefit when compared with placebo. When the results of all published placebo-controlled trials are pooled the typical improvement in smoking cessation rate is 40% (odds ratio continued smoking 0.6; 95% confidence interval 0.5-0.71; P less than 0.00001). The best results with nicotine chewing gum have been obtained with multicomponent programmes which have included some counselling and ongoing follow up and support. Early reports of success with a transdermal nicotine preparation suggest that it may have similar efficacy to nicotine gum. Clonidine administered orally or transdermally has also been shown to reduce tobacco withdrawal symptoms but requires more convincing evidence of long-term efficacy before it can be recommended for routine use. Currently available over-the-counter products, apart from nicotine chewing gum, have not been shown to be effective.
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PMID:Antismoking products. 224 97

Elevated elastase activity in patients with chronic obstructive pulmonary disease (COPD) is attributable to the direct effect of nicotine. COPD is also known to be an independent predictor of abdominal aortic aneurysm (AAA) growth and rupture. The purpose of this study is to determine the effect of nicotine on elastase activity release from neutrophils of AAA patients. Human neutrophils were extracted from the blood of subjects in the following six groups, n = 10 in each group: smoking AAA (SAAA), nonsmoking AAA (NSAAA), smoking aortic occlusive disease (SAOD), nonsmoking aortic occlusive disease (NSAOD), smoking controls (SC), and nonsmoking controls (NSC). After incubation with varying nicotine concentrations (0-1000 microg/ml), the released elastase activity was determined. There is generally an elevation in elastase activity release by neutrophils of smokers compared to nonsmokers. Nicotine exposure stimulated increased elastase activity release in AOD and AAA, and the increase was especially pronounced in the SAAA and SAOD groups. The elevation was greatest in the SAAA group while the release was lowest in the NSAOD group. There is a direct correlation between elastase activity release and nicotine concentration. The data suggest that COPD and AAA development, which may occur by similar initial mechanisms may also be aggravated by nicotine-induced neutrophil elastase activity release. In addition, the results indicate that nicotine is playing an active role in the development of vascular disease by inducing neutrophils to release elastase activity.
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PMID:Nicotine-stimulated elastase activity release by neutrophils in patients with abdominal aortic aneurysms. 945 95

Cigarette smoking is among the leading risk factors in the etiology of atherosclerotic vascular disease. The mechanism, however, that links cigarette smoking to an increased incidence of atherosclerosis is poorly understood. Endothelial cell (EC) integrity is critical in preventing vascular lesion formation, and after a loss of EC integrity reendothelialization must be rapid and complete. We therefore investigated whether cigarette smoke affected the ECs ability to migrate or altered the intracellular signals generated during migration. The DMSO-soluble fraction of cigarette smoke condensate (CSC), derived from the standard research cigarette, was tested on cultured ECs (HUVEC) derived from human umbilical vein. The addition of CSC caused a dose-dependent decrease in the ability of EC to migrate as measured over a 24-h time period. Nicotine and cadmium sulfate, two constituents of cigarette smoke, individually or in combination, had no effect on migration. Examination of the tyrosine phosphorylation state of various intracellular proteins by Western blot analysis showed that CSC caused the hyperphosphorylation of a 130-kDa protein. In addition, other intracellular proteins showed changes in their phosphorylation states after CSC addition. These results support the hypothesis that CSC is detrimental to normal EC function in maintaining vascular integrity and suggest that smokers are more likely to develop complications of vascular disease due to delayed or incomplete reendothelialization as a consequence of decreased EC migration.
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PMID:Inhibition of endothelial cell migration by cigarette smoke condensate. 1118 Sep 90

Although smoking is one of the major risk factors for the development of atherosclerosis, the exact mechanism of smoking-related vascular disease is not known. Smoking causes acute hemodynamic alterations such as increase in heart rate, systemic and coronary vascular resistance, myocardial contractility, and myocardial oxygen demand. These short-term effects could lower the ischemic threshold in smokers with coronary artery disease and contribute to the increased risk for acute cardiovascular events. Endothelial damage is thought to be an initiating event in atherosclerosis and early studies have demonstrated that long-term smoking has direct toxic effects with structural changes of human endothelial cells. Recent research has shown the importance of the functional role of the endothelium in regulating normal vascular tone, platelet-endothelial interactions, leukocyte adhesion and smooth muscle cell proliferation via synthesis and release of a variety of substances such as nitric oxide. There is strong evidence that smoking leads to endothelial dysfunction in both conductance and resistance vessels. This effect seems to be dose-related and reversible. The mechanism of endothelial dysfunction in smokers is not known, but increased degradation of nitric oxide by oxygen-derived free radicals has been suggested. In addition, smoking could cause oxidative inactivation of tetrahydrobiopterin, a critical cofactor of nitric oxide, leading to an uncoupling of the endothelial nitric oxide synthase with increased superoxide production and decreased nitric oxide bioactivity. Other pro-atherosclerotic effects of smoking are discussed. Given the enormous health hazard of tobacco use, complete abstinence from smoking should be achieved. Smoking cessation counseling should be given to healthy subjects and even more vigorously to patients with manifested disease. Every effort should be undertaken to prevent children and adolescents from starting to smoke. Brief tobacco dependence treatment is effective, and every tobacco user should be offered at least brief treatment at every office visit. More intensive treatment is more effective in producing long-term abstinence from tobacco. Nicotine replacement therapy (nicotine patches or gum), clinician-delivered social support, and skills training are the three most effective components of smoking cessation treatment.
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PMID:[Primary and secondary prevention of coronary heart disease: smoking]. 1243 60

Smoking is the leading preventable cause of illness and premature death in Germany, claiming over 110,000 lives a year because it directly increases the risk of dying from heart disease, stroke, emphysema and a variety of cancers. The overwhelming majority of smokers begin tobacco use before they reach adulthood. Among those young people who smoke, the average age is now 13-14. In Germany, about 39% of male and 31% of female adults (age 18-60 years) continue to smoke, despite information about the unequivocally negative health consequences of smoking. The exact mechanisms of smoking-related vascular disease are not yet known. Smoking causes acute hemodynamic alterations such as increase in heart rate, systematic and coronary vascular resistance, myocardial contractility, and myocardial oxygen demand. These short-term effects could lower the ischemic threshold in smokers with coronary artery disease and contribute to the increased risk for acute cardiovascular events. Endothelial damage is thought to be an initiating event in atherosclerosis and early studies have demonstrated that long-term smoking has direct toxic effects with structural changes of human endothelial cells. Recent research has shown the importance of the functional role of the endothelium in regulating vascular tone, platelet-endothelial interactions, leukocyte adhesion and smooth muscle cell proliferation via synthesis and release of a variety of substances such as nitric oxide. There is strong evidence that smoking leads to endothelial dysfunction mainly by increased inactivation of nitric oxide by oxygen-derived free radicals. Smoking also increases oxidative modification of LDL and is associated with lower HDL plasma levels. Smoking induces a systemic inflammatory response with increased leukocyte count and elevation of the C-reactive protein level. Importantly, the prothrombotic effects of smoking have been repeatedly demonstrated to cause alterations in platelet function, imbalance of antithrombotic vs prothrombotic factors, and decrease of fibrinolytic activity. Given the enormous health hazard of tobacco use, complete abstinence from smoking should be achieved. Smoking cessation counselling should be given to healthy subjects and even more vigorously to patients with manifested disease. Every effort should be undertaken to prevent children and adolescents from starting to smoke. Brief tobacco dependence treatment is effective, and every smoker should be offered at least brief treatment at every office visit. More intensive treatment is more effective in producing long-term abstinence from tobacco. Nicotine replacement therapy (nicotine patches or gum), clinician-delivered social support, and skills training are the three most effective components of smoking cessation treatment. A framework for tobacco control measures is necessary to reduce tobacco consumption and exposure to tobacco smoke. Recommendations on specific tobacco control interventions are: 1. increase in tobacco taxes; 2. comprehensive tobacco advertising bans; 3. legislation prohibiting smoking in work and public places; 4. prohibiting the sales of tobacco products to persons under 18; 5. comprehensive disclosure of the physical, chemical and design characteristics of all tobacco products; 6. training of health professionals to promote smoking prevention and cessation interventions; and 7. development of a national network of smoking cessation treatment services.
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PMID:[Prevention of coronary heart disease: smoking]. 1625 91

Atherosclerosis and neointimal hyperplasia formation are induced by alterations in the homeostatic balance between cell growth and cell death. Apoptosis is a physiological cell death process that, when deregulated, may be involved in many pathological conditions. Cigarette smoking is a primary risk factor for vascular disease and nicotine seems to exert its atherogenic effects in part through the increase of smooth muscle cell (SMC) proliferation. The aim of this study was to investigate the effect of nicotine on SMC apoptosis. Nicotine added for 24 and 72 h to serum deprived cell cultures resulted in a decrease of apoptotic SMCs. The inhibition was direct and not mediated by platelet-derived growth factor, basic fibroblast growth factor, and transforming growth factor beta(1), autocrinally released by nicotine-treated SMCs, because it was not influenced by addition of specific neutralizing antibodies. Apoptosis inhibition as well as the proliferation increase, and basic fibroblast growth factor expression on nicotine-treated SMCs were blocked by nicotinic acetylcholine receptor antagonists, including alpha-bungarotoxin, a competitive antagonist of alpha subunits of nicotinic receptor. In conclusion, we propose that nicotine could lead to the increase of neointimal SMCs in vascular lesions by inducing the inhibition of physiological SMC apoptosis and the increase of SMC proliferation. We also showed that nicotine signaling occurs as a result of activation of the classical nicotine receptor pathways.
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PMID:Nicotine inhibits apoptosis and stimulates proliferation in aortic smooth muscle cells through a functional nicotinic acetylcholine receptor. 1846 30

Nicotine and soluble semi-stable aldehydes and ketones in cigarette smoke are key mediators of the elevated risks for vascular disease, cancer, and chronic obstructive pulmonary disease observed in smokers. Nicotine, via sympathetic stimulation, increases risk for both vascular disease and cancer. Comprehensive suppression of sympathetic activity with the well-tolerated drug carvedilol, which inhibits betal 1, beta2 and alphal adrenergic receptors, may be protective to smokers and other nicotine addicts. The soluble aldehydes and ketones in tobacco smoke appear to exert their adverse effects through activation of NADPH oxidase complexes in vascular tissues and in the lungs. The phytochemical phycocyanobilin (PhyCB), richly supplied by the edible cyanobacterium spirulina, in studies on rodents and in human cell cultures has shown the ability to safely mimic intracellular bilirubin's physiological role as an inhibitor ofNADPH oxidase activity. It therefore may have potential for mitigating the pro-oxidative effects of tobacco smoke aldehydes and ketones. Joint administration of carvedilol and spirulina merits exploration as a strategy for moderating the pathogenic impact of smoking in chronic tobacco users who either fail to quit or refuse to try cessation of tobacco. Carvedilol may be appropriate for those who manage a nicotine addiction in other ways (smokeless tobacco, e-cigarettes, nicotine gum). Further clinical studies to evaluate the impact of carvedilol on cardiovascular risk factors in nicotine addicts, and rodent studies to assess markers of lung inflammation in smoke- exposed rodents fed PhyCB, are recommended.
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PMID:Carvedilol and spirulina may provide important health protection to smokers and other nicotine addicts: a call for pertinent research. 2581 81

Abdominal aortic aneurysm (AAA) is a vascular disease involving gradual dilation of the abdominal aorta. Recent studies suggest that nicotine, which is a primary component in cigarette smoke, is closely associated with the development and rupture of an AAA. Nicotine accelerates AAA development through the weakening of the vascular wall by increasing oxidative stress and matrix metalloproteinase (MMP)-2 expression. However, little is known about preventing the AAA induced by nicotine. A non-surgical means of preventing the weakening of the vascular wall before the onset of AAA by functional food factors would be a valuable option over surgery. Fish oil is a functional food that is rich in n-3 polyunsaturated fatty acids that have an anti-inflammatory effect. In this study, we evaluated the effect of dietary fish oil on the weakening of the aortic wall due to nicotine administration in a mouse model. Histological analysis showed that the dietary fish oil suppressed the degradation of elastin fibers in the nicotine-administered mice. Additionally, the dietary fish oil suppressed the protein level of MMP-12, macrophage infiltration, and the oxidative stress in the vascular wall. These results suggest that fish oil could suppress the weakening of the vascular wall by suppressing the elastin fiber degradation caused by nicotine. By suppressing the nicotine induced weakening of the vascular wall, fish oil might help prevent the development of AAA.
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PMID:Suppressive effects of dietary EPA-rich fish oil on the degradation of elastin fibers in the aortic wall in nicotine-administered mice. 2872 3

Abdominal aortic aneurysm (AAA) is a vascular disease characterized by the weakening of the vascular walls and the progressive dilation of the abdominal aorta. Nicotine, a primary component of cigarette smoke, is associated with AAA development and rupture. Nicotine induces AAA development by weakening vascular walls. However, little is known about preventive methods using functional food factors for nicotine-induced vascular destruction. Sesamin and sesamolin are functional food factors that are fat-soluble lignans found in Sesamum indicum seeds. Previous reports indicated that sesamin and sesamolin have anti-oxidative and anti-inflammatory effects. In this study, we evaluated the effects of sesamin and sesamolin-rich sesame extract on the weakening of vascular walls in nicotine-administered mice. Sesame extract attenuated the degradation of collagen and elastin fibers caused by nicotine. In addition, sesame extract decreased the area positive for matrix metalloproteinase 12 (MMP-12) and oxidative stress in the vascular walls. These results suggest that sesame extract may decrease the weakening of vascular walls by suppressing the nicotine-induced degradation of collagen and elastin fibers. Sesame extract may be effective in preventing AAA development by decreasing both, MMP-12 expression and oxidative stress in vascular walls.
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PMID:Sesame Extract Attenuates the Degradation of Collagen and Elastin Fibers in the Vascular Walls of Nicotine-administered Mice. 3060 56


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