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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The literature points out the meaning of risk factors causing stroke as well as their therapy or elimination as an effective prevention of cerebrovascular disease. Hypertension increases the risk of apoplexy by 4-fold, with regard to the diastolic values of blood pressure by the 5-fold up to the 10-fold. Consistent hypertension therapy decreases significantly the incidence of cerebral apoplectic attacks. Manifested diabetes mellitus and even reduced glucose tolerance raise the risk of stroke by the 3-fold, even though factors frequently associated with diabetes are taken into consideration. Hyperlipidemia, hypercholesteremia, and hypertriglyceridemia stipulate an increase of stroke incidence by the 2-fold to the 3-fold. Morbidity rate rises if these abnormalities coincide with further risk factors, up to the 6-fold. Nicotine consumption alone increases the risk of cerebral apoplectic attacks in relation to age, by the 3-fold up to the 5-fold. In combination with the use of hormonal contraceptive drugs, the risk of morbidity rate in women rises to the 7-fold. Overweight of more than 30% aggravates twice the risk of stroke. Heart diseases of different kind increase the risk of apoplectic attacks by the 2-fold, in combination with hypertension by the 5-fold. The intake of oral contraceptives (OCs) causes an increase of cerebral thromboembolic attacks by the 3-fold up to the 5-fold, whereby a relation to estrogen content and to hemorheology disturbances is proven. Blood coagulation disturbances, especially hypercoagulability with increase of blood level of fibrinogen, fibrin, and enhanced adhesiveness of thrombocytes in cerebrovascular disease are proven to be valid. By combination of various risk factors apoplexy risk is additionally increased. The possibility of surgical and neurosurgical prophylactic treatment in all stages of cerebral ischemia, caused by occlusive disease of the cartoid, vertebral, and intracranial arteries, exists in 75% of patients. With regard to the longterm results of patients with extraintracranial bypass surgery, due to stenosis or occlusion of the carotid artery in its high cervical or intracranial course, or of the middle cerebral artery, the operated group clearly was better than the nonoperated group in frequency of cerebral ischemia recurrence. The therapeutic effect of inhibitors of thrombocytic aggregates and of anticoagulants for the chemotherapeutic prevention of cerebral ischemia, is proven for acetylsalicylic acid and derivatives of coumarin. Both diminish significantly the rate of cerebral ischemia when compared with placebo-treated control groups.
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PMID:[Prevention of cerebrovascular circulatory disorders]. 404 14

In the present study the influence of low doses of intravenous nicotine administration on hormonal and metabolic events was studied in man in view of the clinical implications of moderate smoking on the development of hyperlipidemia. Hormonal, metabolic and cardiovascular effects of a 30 min intravenous nicotine infusion (0.25 or 0.5 microgram/kg/min) were determined in seven non-smoking, healthy, normal weight male individuals after an overnight fast. Nicotine caused a significant dose-dependent increase in the plasma levels of nicotine, cotinine, noradrenaline, adrenaline, glycerol and free fatty acids (FFA). The serum nicotine concentrations peaked at the end of the infusion followed by a gradual decline, although they were still increased 90 min after cessation of infusion. Serum cotinine levels (the main nicotine metabolite) continuously increased during the experiment and statistically significant increases were found from 30 min after the start of infusion of nicotine. Serum noradrenaline, adrenaline, glycerol and FFA levels had increased significantly by 15 min of nicotine infusion. Nicotine produced significant elevations of adrenaline, glycerol and FFA concentrations at both doses (maximal increments of 247, 184 and 153%, respectively) and the peak effect occurred at 30 min. However, noradrenaline levels only responded to the high nicotine dose and the maximal increment (168%) was already found at 15 min. The increments of noradrenaline and adrenaline failed to elicit changes in systolic and diastolic blood pressure or heart rate. Nicotine did not alter plasma levels of glucagon, insulin, glucose, pyruvate or lactate and a non-significant increase in serum cortisol and growth hormone levels was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in circulating lipid and carbohydrate metabolites following systemic nicotine treatment in healthy men. 811 70

Modifications by hyperlipidemia of endothelium-dependent and -independent relaxations were evaluated in cerebral and temporal arteries from control and hyperlipidemic (high cholesterol-fed) monkeys. Histologically atherosclerotic lesions were not observed in either group. Relaxations induced by histamine, abolished by N(G)-nitro->L-arginine (>L-NA), were significantly potentiated in the hyperlipidemic monkey cerebral arteries, compared with those in the arteries from control monkeys. Treatment with superoxide dismutase did not affect the histamine-induced relaxation. Conversely, endothelium-dependent relaxations induced by A23187, Ca2+ ionophore, in cerebral arteries did not differ between control and hyperlipidemic monkeys. In temporal arteries, relaxations by acetylcholine and A23187 did not differ between control and hyperlipidemic monkeys. Endothelium-dependent and -independent relaxations by adenosine diphosphate in cerebral and temporal arteries were not affected by hyperlipidemia. Endothelium-independent relaxations by exogenously applied nitric oxide did not differ in the arteries from control and hyperlipidemic monkeys. Nicotine-induced relaxations in cerebral arteries, which were mediated with nitric oxide released from nitroxidergic (nitrergic) nerves, and the contractions caused by nicotine in temporal and mesenteric arteries treated with >L-NA did not differ between control and hyperlipidemic monkeys. It is concluded that long exposure to hyperlipidemia did not affect endothelial functions of monkey middle cerebral and temporal arteries but enhanced nitric oxide-mediated relaxations caused by histamine, possibly due to upregulation of endothelial histamine receptor-mediated functions in the cerebral arteries. The nitroxidergic (nitrergic) and adrenergic nerve functions do not seem to be affected by hyperlipidemia.
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PMID:Endothelial and neuronal functions in cerebral and temporal arteries from monkeys fed a high-cholesterol diet. 1219 32

Nicotine, a major toxic component of cigarette smoke, plays a key role in the development of cardiovascular disease and lung cancer. In the present study, we have synthesized an analog of curcumin and biomonitored its influence over biochemical marker enzymes and lipid profiles on nicotine-induced toxicity in Wistar rats. The effects were compared with that of curcumin, a well-known antioxidant and anti-hyperlipidemic agent. Toxicity was induced by subcutaneous injection of nicotine at a dose of 2.5 mg/kg of body weight (5 days a week, for 22 weeks), and curcumin (80 mg/kg) was given simultaneously along with nicotine by intragastric intubation for 22 weeks. Measurements of activities of the biochemical marker enzymes aspartate transaminase, alanine transaminase, alkaline phosphatase, and lactate dehydrogenase and of plasma lipid profiles were used to monitor the anti-hyperlipidemic effects of curcuminoids. In nicotine-treated rats, enhanced plasma marker enzymes and lipid profiles were observed. Administration of curcumin or curcumin analog to nicotine-treated rats significantly reduced the activity of marker enzymes and plasma lipid levels. Thus, our findings suggest that curcumin and its analog exert an anti-hyperlipidemic effect against nicotine-induced lung toxicity and may be a promising agent for treatment of hyperlipidemia and atherosclerosis.
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PMID:Modulatory effects of curcumin and curcumin analog on circulatory lipid profiles during nicotine-induced toxicity in Wistar rats. 1611 19

Smoking has been known to cause endothelial dysfunction and is an important risk factor for ischemic stroke. In our study we investigated whether chronic cigarette smoking affects the cerebral blood flow velocity response to a physiological, visual stimulus. By using a visual cortex stimulation paradigm, the flow velocity response in the posterior cerebral arteries (PCA) was measured bilaterally, in 32 young healthy adults (16 smokers, 16 nonsmokers). The stimulation protocol consisted of 10 cycles with a resting phase of 20 s and a stimulating phase of 40 s for each cycle. Besides functional transcranial Doppler (TCD), laboratory tests and measurement of intima-media-thickness (IMT) were also performed. Repeated-measure analysis of variance (ANOVA) was used to detect differences in visually evoked relative flow velocity time courses between smokers and nonsmokers. Repeated-measure ANOVA revealed marked difference in the peak systolic flow velocity time courses between smokers and nonsmokers (p< .001). Maximum percent change of visually evoked flow velocity after visual stimulation was 19+/-4% and 30+/-3% in smokers and nonsmokers, respectively (p< .0001). IMT values did not indicate atherosclerosis in young smokers. Infectious disease and hyperlipidemia were also ruled out by measurement of sensitive C-reactive protein and serum lipids. This is the first functional TCD study demonstrating impaired visually evoked flow velocity response caused by chronic cigarette smoking in otherwise healthy, young subjects. The impaired cerebral vasodilatory mechanism together with atherosclerosis may influence stroke occurrence and outcome in chronic smokers.
Nicotine Tob Res 2008 Feb
PMID:Visually evoked cerebral vasomotor response in smoking and nonsmoking young adults, investigated by functional transcranial Doppler. 1823

The effect of two different doses (1 microg Se/Kg and 50 microg Se/Kg Body wt) of selenium on nicotine induced hyperlipidemia was investigated in rats. Results revealed that nicotine intake caused an increase in concentration of cholesterol, triglycerides, free fatty acids, phospholipids and low density lipoprotein compared to control group. Coadministration of selenium along with nicotine reduced the levels of lipids compared to nicotine group. This reduction was due to reduction in the biosynthesis of lipids as evidenced by the reduced activity of HMGCoA reductase and lipogenic enzymes. Nicotine intake also reduced the absorption of selenium in the intestine. Histopathological studies revealed that selenium at a dose of 1 microg was more effective in reducing lipid levels and higher dose of selenium was toxic.
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PMID:Effect of exogenous selenium on nicotine induced hyperlipidemia in rats. 1913 Aug 56

Cigarette smoking continues to pose a significant health burden on society. Two well-described mechanistic links associating smoking with morbidity and mortality include elevated blood lipids and increased oxidative stress. These variables have traditionally been measured while an individual is fasting, but evidence suggests that postprandial lipemia and oxidative stress provide more important information concerning susceptibility to disease, in particular cardiovascular disease. Cigarette smokers have elevated levels of biomarkers of oxidative stress at rest and experience impaired postprandial lipid and glucose metabolism. We have confirmed these findings while noting an exaggerated oxidative stress response to high-fat feeding. Smoking cessation is without question the best approach to minimizing smoking-induced ill health and disease, but success rates among those who attempt to quit are dismal. Other means to decrease a smoker's susceptibility to oxidative stress-related disease are needed. We propose that exercise may aid in attenuating postprandial oxidative stress, and we do so in 3 distinct ways. First, exercise stimulates an increase in endogenous antioxidant enzyme activity. Second, exercise improves blood triglyceride clearance via a reduced chylomicron-triglyceride half-life and an enhanced lipoprotein lipase activity. Third, exercise improves blood glucose clearance via an enhanced glucose 4 transport protein translocation and protein content, as well as insulin-insulin receptor binding and postreceptor signaling. Improvements in antioxidant status, as well as lipid and glucose processing, may aid greatly in minimizing feeding-induced oxidative stress in smokers. If so, and in accordance with the recent joint initiative of the American College of Sports Medicine and the American Medical Association, exercise may be viewed as a "medicine" for cigarette smokers at increased risk for postprandial oxidative stress. Research into this area may provide insight into the potential benefits of exercise for this purpose.
Nicotine Tob Res 2009 Jan
PMID:The role of exercise in minimizing postprandial oxidative stress in cigarette smokers. 1924 36

Nicotine, an active ingredient of tobacco smoke, is known to induce hyperlipidemia and disturb the prooxidant-antioxidant status. In our study, ferulic acid, a naturally occurring nutritional compound, was tested for its antioxidant and antihyperlipidemic property in a dose-dependent manner against nicotine-induced toxicity in female Wistar rats. We tested three different doses of ferulic acid-10 mg, 20 mg, and 40 mg/kg body weight-for their protective effects. The activities of biochemical marker enzymes lactate dehydrogenase and alkaline phosphatase, levels of peroxidative indices (thiobarbituric acid reactive substances and hydroperoxides), nitric oxide, and circulatory lipids (cholesterol, triglycerides, free fatty acids, and phospholipids) were increased significantly in the nicotine-treated group when compared to normal, which were brought down in ferulic acid-treated groups. The antioxidant status (superoxide dismutase, catalase, glutathione peroxidase, vitamin E, and reduced glutathione) was found to be decreased in the nicotine-treated group, and was significantly increased in ferulic acid-administered groups. Further, ferulic acid also positively modulated the nicotine-induced changes in the micronutrients (zinc and copper) level. The dose 20 mg/kg body weight was found to be more effective than the other two doses. Our data suggest that FA exerts its preventive effects by modulating the degree of lipid peroxidation, antioxidant status, lipid profiles, and trace element levels during nicotine-induced toxicity.
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PMID:Ferulic Acid modulates altered lipid profiles and prooxidant/antioxidant status in circulation during nicotine-induced toxicity: a dose-dependent study. 2002 Oct 59

Nicotine may contribute to accelerated atherogenesis by inducing hyperlipidemia, injuring endothelial cells, and/or promoting thrombosis, although the evidence is not conclusive. Nicotine is likely to contribute to acute ischemic events in people who already have coronary heart disease via adverse effects on systemic hemodynamics, by promoting thrombosis, constricting coronary arteries, and/or facilitating arrhythmogenesis. Pharmacodynamic studies suggest that nicotine inhaled in cigarette smoke may have different cardiovascular effects than that absorbed more slowly, as from nicotine gum or transdermally. The safety of chronic nicotine exposure, such as with medicinal use of nicotine, cannot be predicted and requires empiric evaluation.
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PMID:Nicotine and coronary heart disease. 2123 86

Nicotine is a parasympathomimetic alkaloid present in tobacco which can induce hyperlipidemia and has a direct effect on neural functions. Statins, competitive inhibitors of 3-hydroxymethyl-3-glutaryl-coenzyme-A reductase, are cholesterol lowering drugs. It has some neuroprotective effects. Hence we analysed the combined effect of nicotine and statin on the learning behaviour of male albino rats. We employed Y-Maze conditional discrimination task. Rats were divided into 4 groups with six rats in each group. (1) Control, (2) Atorvastatin (10mg/kgb.wt), (3) Nicotine (0.6mg/kgb.wt) and (4) Atorvastatin (10mg/kgb.wt)+Nicotine (0.6mg/kgb.wt). After 30days of treatment rats from each group were selected for behavioural study and they were observed for 30days. At the end of the experimental period rats were sacrificed, and brain and liver were dissected out for further biochemical analysis. Nicotine treated group showed least performance in learning in comparison with control, atorvastatin and atorvastatin+nicotine treated groups. Co-administration of atorvastatin and nicotine improved learning behaviour compared to nicotine treated group. Reactive oxygen species level was significantly increased in nicotine group compared to control. The level of neurotransmitter serotonin which has a significant role in learning was found to be decreased in nicotine treated group compared to the control group. Activity of Na(+) K(+) ATPase, Ca(2+) ATPase and glutathione content was significantly reduced in nicotine treated group compared to control. The activity of acetylcholine esterase was significantly increased in the nicotine treated group. Expression studies showed significant decrease in N-methyl D-aspartate receptors and increase in mono amine oxidase-A and mono amine oxidase-B in nicotine treated group and was reversed in atorvastatin + nicotine treated group. It can be concluded that co-administration of nicotine with statin ameliorates the neural functional alterations caused by nicotine to a significant level.
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PMID:Atorvastatin improves Y-maze learning behaviour in nicotine treated male albino rats. 2640 79


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