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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tobacco smoking has been reported to be associated with increased risk of cardiovascular disease and cancer, particularly of the lungs. In spite of extensive research on the health effects of tobacco smoking, the substances in tobacco smoke exerting these negative health effects are not completely known. Nicotine is the substance giving the subjective pleasure of smoking as well as inducing addiction. For the first time we report the effect on the rat of long-term (two years) inhalation of nicotine. The rats breathed in a chamber with nicotine at a concentration giving twice the plasma concentration found in heavy smokers. Nicotine was given for 20 h a day, five days a week during a two-year period. We could not find any increase in mortality, in atherosclerosis or frequency of tumors in these rats compared with controls. Particularly, there was no microscopic or macroscopic lung tumors nor any increase in pulmonary neuroendocrine cells. Throughout the study, however, the body weight of the nicotine exposed rats was reduced as compared with controls. In conclusion, our study does not indicate any harmful effect of nicotine when given in its pure form by inhalation.
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PMID:Long-term effects of inhaled nicotine. 861 91

Nicotine, a major component of cigarette smoke, plays an important role in the development of cardiovascular disease and lung cancer in smokers. Lipid peroxidation is a process associated with the pathogenesis of atherosclerosis and the level of lipid peroxides is increased in smokers. In rats fed a high-fat diet, the tissue concentration of lipid peroxides was found to be increased. On nicotine administration along with a high-fat diet an additive effect was observed in lipid peroxidation and free radical scavengers. The activities of scavenging enzymes superoxide dismutase, catalase and glutathione reductase were found to be decreased, while the glutathione concentration and activity of glutathione peroxidase were enhanced.
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PMID:Effect of nicotine on antioxidant defence mechanisms in rats fed a high-fat diet. 884 84

Cigarette smoking has been established as a major risk factor for atherosclerosis and also for lung cancer. Nicotine is one of the major toxic components of cigarette smoke that is believed to be partly responsible for the deleterious effect of cigarette smoke. Alcohol intake is another major risk factor for the development of cardiovascular disease. Lipid peroxidation is a process associated with the pathogenesis of atherosclerosis. The concentration of lipid peroxides is found to be increased in alcohol-treated rats. On nicotine administration along with alcohol, an additive effect was observed in lipid peroxidation and the antioxidant defence mechanism. The activity of scavenging enzymes superoxide dismutase, catalase and glutathione reductase was found to be decreased, while the activity of glutathione peroxidase and the concentration of glutathione were increased.
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PMID:Additive effect of alcohol and nicotine on lipid peroxidation and antioxidant defence mechanism in rats. 885 16

Nicotine activates the sympathetic nervous system and in this way could contribute to cardiovascular disease. Animal studies and mechanistic studies indicate that nicotine could play a role in accelerating atherosclerosis, but evidence among humans is too inadequate to be definitive about such an effect. Almost certainly, nicotine via its hemodynamic effects contributes to acute cardiovascular events, although current evidence suggests that the effects of nicotine are much less important than are the prothrombotic effects of cigarette smoking or the effects of carbon monoxide. Nicotine does not appear to enhance thrombosis among humans. Clinical studies of pipe smokers and people using transdermal nicotine support the idea that toxins other than nicotine are the most important causes of acute cardiovascular events. Finally, the dose response for cardiovascular events of nicotine appears to be flat, suggesting that if nicotine is involved, adverse effects might be seen with relatively low-level cigarette exposures.
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PMID:The role of nicotine in smoking-related cardiovascular disease. 924 58

Cardiovascular complications are the main cause of death in hypertensive patients. They occur more often in tobacco smokers. The effect of nicotine activity is insulin resistance leading to lipid disorders which are risk factor for atherosclerosis. Smoking and hypertension intensify the atherogenic effect of each other. The risk of ischaemic heart disease in a hypertensive smoker is almost 3.5 times greater than in a non-smoker with normal blood pressure at the same serum cholesterol concentration. Nicotine multiplies the risk of cardiovascular complications caused by left ventricular hypertrophy in arterial hypertension. Strokes (ischaemic strokes and subarachnoid haemorrhages) are more common in smokers. Smokers also develop accelerated malignant hypertension more frequently than non-smokers. Smoking is also a risk factor for renal artery stenosis, both atheromatous and fibromuscular.
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PMID:[Nicotine and cardiovascular complications of chronic hypertensive disease]. 969 47

Nicotine is reported to have toxic effects on gonadal functions, in addition to its established role in the pathogenesis of atherosclerosis and lung cancer. So nicotine-induced biochemical changes were studied in liver and testes. Chronic administration of nicotine was found to produce enhanced synthesis of cholesterol, triglycerides, phospholipids and free fatty acids in the liver and testes. The activity of the lipogenic enzymes was high in liver but unaltered in testes. The testosterone and estradiol levels in the serum were lower. As the changes brought about by chronic administration of nicotine were counteracted by mecamylamine, a known inhibitor of nicotine, it was proven that nicotine is having a specific gonadotoxic effect.
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PMID:Nicotine administration induced changes in the gonadal functions in male rats. 983 25

Nicotine, a constituent of cigarette smoking, may induce atherosclerosis through the production of growth factors. The pattern of bFGF and TGF beta1 production and release by bovine aortic endothelial cells (EC) stimulated with nicotine (from 6 x 10(-4) to 6 x 10(-8) M) was studied. EC viability and count were assessed. The presence of bFGF and TGF beta1 in serum-free conditioned media was determined by the inhibition antibody-binding assay and Western blot analysis. Mitogenic activity of nicotine on EC was also determined. Polymerase chain reaction (PCR) was used to study the expression of bFGF and TGF beta1. The bFGF release after nicotine stimulation was greater than controls, whereas TGF beta1 release was lower. At a nicotine concentration of 6 x 10(-6) M we noted the greatest mitogenic activity. The addition of monoclonal antibody anti-bFGF decreased the tritiated thymidine uptake of EC exposed to nicotine but the addition of monoclonal antibody anti-TGF beta1 had no significant effect. bFGF mRNA expression was significantly higher in EC exposed to nicotine than in controls, whereas TGF beta1 mRNA expression was not modified. From these data we concluded that nicotine regulates bFGF production and release and TGF beta1 release and may have a key role in the development and progression of atherosclerosis.
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PMID:Nicotine regulates basic fibroblastic growth factor and transforming growth factor beta1 production in endothelial cells. 1019 8

Nicotine, a major component of tobacco, is partly responsible for the development of atherosclerosis. It has been suggested that antioxidant nutrients are protective against degenerative diseases. So we have studied the antioxidant effect of oils isolated from onion and garlic on nicotine-induced lipid peroxidation in rat tissues. The lipid peroxidation products and scavenging enzymes were assessed in liver, lungs, heart and kidney. The rats were treated with 0.6 mg nicotine/kg bw and simultaneously given 100 mg garlic or onion oils/kg bw for 21 d. Thiobarbituric acid reactive substances, conjugated dienes and hydroperoxides concentrations were significantly increased in the tissues of nicotine-treated rats. Both the garlic oil and onion oil supplementation to nicotine-treated rats increased resistance to lipid peroxidation. The activities of catalase, superoxide dismutase and glutathione peroxidase decreased in nicotine-treated rats, but there was a trend to increased glutathione content. With garlic oil or onion oil supplementation, nicotine-treated rats had increased activities of antioxidant enzymes and increased concentrations of glutathione. These results indicate that oils of garlic and onion are effective antioxidants against the oxidative damage caused by nicotine.
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PMID:Antioxidant role of oils isolated from garlic (Allium sativum Linn) and onion (Allium cepa Linn) on nicotine-induced lipid peroxidation. 1050 36

Despite the fact that the epidemiological evidence linking cigarette smoking with cardiovascular disease is overwhelming, the precise components of cigarette smoke responsible for this relationship and the mechanisms by which they exert their effect have not yet been elucidated. There are however, some promising pointers as a result of recent developments and this review concentrates on new evidence since earlier reviews of this topic. It is now known that the endothelium has a vastly more important role than was ever thought to be the case a decade ago. Its role in health and disease is increasingly understood, as is the relationship between endothelial injury and the development of atherosclerosis. There is considerable evidence that cigarette smoking can result in both morphological and biochemical disturbances to the endothelium both in vivo and in cell culture systems. Cigarette smoke is a complex mixture and only a few components have been extensively studied. Nicotine and carbon monoxide are much less damaging than is whole smoke. However the free radical components of cigarette smoke have been shown to cause damage in model systems. Further work will be necessary to consolidate the evidence base but the data reported in this review suggest that the free radical components of cigarette smoke may be responsible for the morphological and functional damage to endothelium that has been observed in model systems.
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PMID:Cigarette smoking, endothelial injury and cardiovascular disease. 1097 43

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


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