Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The content of 10 trace elements was studied by employing the neutron-activation method and the lead level determined through the spectral analysis in the whole blood, aorta, the heart muscle, liver, intesties (small and large), in the pancreas, adrenal glands, the spleen, lungs of accident victims, among whom 87 were practically healthy and 91 had atherosclerosis. The latter demonstrated in a number of organs (especially in the aorta and liver) a reduction in the content, which increased with age and intensity of atherosclerotic changes, of nickel, manganese, zinc, cobalt, vanadium and iron and rise in the lead, gallium, copper, bismuth and bromine level. The disclosed data bear witness to a definite part played by a number of trace elements in the atherogenesis.
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PMID:[Trace element content in the blood and organs in arteriosclerosis]. 123 10

Nickel was measured, by electrothermal atomic absorption spectrophotometry, in sera from (a) 30 healthy adults, (b) 54 patients with acute myocardial infarction, (c) 33 patients with unstable angina pectoris without infarction, and (d) five patients with coronary atherosclerosis who developed cardiac ischemia during treadmill exercise. Mean (and SD) concentrations in Group a were 0.3 (0.3) microgram/L (range less than 0.05-1.1 microgram/L). Within 72 h after hospital admission, hypernickelemia (Ni greater than or equal to 1.2 microgram/L) was found in 41 patients of group b (76%) and in 16 patients of group c (48%). Hypernickelemia was found before and after exercise in one patient of Group d (20%). Peak values averaged 3.0 micrograms/L (range 0.4-21 micrograms/L) in Group b, 1.5 microgram/L (range less than 0.05-3.3 micrograms/L) in Group c. In Group b, the mean time interval between the peak values for creatine kinase activity and for nickel was 18 h. Serum nickel concentrations were unrelated to age, sex, time of day, cigarette smoking, medications, clinical complications, or outcome. Mechanisms and sources of release of nickel into the serum of patients with acute myocardial infarction or unstable angina pectoris are conjectural, but hypernickelemia may be related to the pathogenesis of ischemic myocardial injury.
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PMID:Nickel concentrations in serum of patients with acute myocardial infarction or unstable angina pectoris. 397 87

During an annual toxicological experiment on white male rats, receiving orally vanadium (V) and nickel (Ni) in doses, equivalent to the accepted in Bulgaria, maximum allowable norms for ist category surface waters (respectively 0.005 mg/kg and 0.0025 mg/kg), 2 and 6 times and 20 and 60 times higher, is studied the atherogenic effect of the latter after the indices: total cholesterol, beta-lipoproteins, phospholipids, lecithin, total lipids, total protein and hexoses of glycoproteins in the serum; oxyproline, hexauranium acids and hexoses, hexosamines, connected with the proteins in the aorta. It is established that V and Ni in chronic combined effect in doses, equivalent to those accepted in Bulgaria, in maximum allowable concentrations for Ist category waters and surpassing them 2 and 6 time respectively, lead to no changes in the biochemical composition of the connective tissue of the aorta and to disorders in the lipidic and protein metabolism, while in higher doses is registered an increase of the glucoproteins and decrease in the glucosaminglycans in the aorta and decrease of the total lipids in the serum. The results point out, that V and Ni in the conditions of the experiment don't accelerate the processes of the natural ageing of the vessels and have no atherogenic effect. Juxtaposing the data for V and Ni concentrations in drinking waters in Bulgaria with our results give grounds to reckon, that their raised content in drinking waters in some regions do not represent a risk factor for the development of atherosclerosis.
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PMID:[An experimental study of the atherogenic effect of the vanadium and nickel contained in drinking water when combined]. 784 74

The Cu, Zn, Cr, Fe, and Ni concentrations from the atherosclerotic plaques in the abdominal aorta obtained from 40 patients who died of coronary heart disease (CHD) were measured. In 32 of them the clinical and anatomical diagnosis was ischemic heart disease (IHD) and in 8 of them it was acute myocardial infarction (AMI). Concomitant determinations of the concentrations of the above trace elements were determined in 16 normal aortas from subjects who died in accidents or from causes other than atherosclerosis (C). The determinations were done by means of a Perkin-Elmer atomic absorption spectrophotometer, Model 300. The results are expressed in mg/kg of dried tissue. The Cu, Zn, and Cr concentrations were significantly lower (p < 0.01) in the atherosclerotic plaques of abdominal aorta of the deceased patients with IHD and AMI than in the control group. Iron had the tendency to rise but not significantly. The nickel level in the atherosclerotic plaques from abdominal aorta did not change significantly as compared to the controls. We attribute the low values of copper in the atherosclerotic aortic tissue in IHD and AMI to a shift of copper from aortic tissue into the blood. At present, there is no explanation for the low concentration of zinc and chromium in atherosclerotic aortic tissue.
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PMID:Concentration of copper, zinc, chromium, iron and nickel in the abdominal aorta of patients deceased with coronary heart disease. 788 Dec 75

Alteration of glycosaminoglycans (GAGs) in cultured bovine aortic smooth muscle cells after exposure to cadmium was investigated. It was revealed that cadmium increased the accumulation of GAGs metabolically labeled with [3H]glucosamine but decreased that with [35S]sulfate in the cell fraction, the cell surface fraction and the medium fraction. This suggested that cadmium stimulated the biosynthesis of GAGs but inhibited their sulfation in the cells. A similar alteration was observed in cadmium-treated human aortic smooth muscle cell layer. Of tested cations including cadmium, bismuth, cobalt, copper, lead, manganese, nickel and zinc, only cadmium stimulated [3H]glucosamine incorporation, with a strong inhibition of the [35S]sulfate incorporation in the bovine cells. Characterization of bovine smooth muscle GAGs showed that the cadmium-induced increase in the [3H]glucosamine incorporation was mainly observed in heparan sulfate; the inhibition of the [35S]sulfate incorporation occurred non-selectively. Cadmium accumulated in bovine vascular smooth muscle cells in a dose-dependent manner with an increase in the leakage of lactate dehydrogenase into the medium. The present data suggest that vascular smooth muscle cells respond to the cytotoxicity of cadmium and promote the GAG synthesis with a reduction of their sulfation. It is postulated that this response may be a defensive one to the damage of the vascular tissue caused by cadmium but would be a component of the metal-induced atherosclerosis.
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PMID:Alteration of glycosaminoglycans induced by cadmium in cultured vascular smooth muscle cells. 799 22

We investigated the effect of serum cholesterol level and stent design on the restenosis rate within the stent after balloon angioplasty and stent implantation using atherosclerotic rabbits. Two types of nickel/titanium stents with gaps (open stent) and without gaps (closed stent) between the wire coils were implanted into the aorta of the rabbits 10 weeks after atherosclerosis had been induced using a standard high cholesterol diet and balloon abrasion. Each rabbit had an open stent and a closed stent implanted into the infrarenal abdominal aorta. Between these two stents a control segment of the aorta was treated with angioplasty alone. The animals were divided into two groups according to the diet protocol as follows: in group I (n = 9) a high cholesterol diet was stopped after stent implantation; in group II (n = 10) a high cholesterol diet was maintained after stent implantation. Digital subtraction angiograms were obtained every 4 weeks for up to 24 weeks and the narrowest diameter of the arterial segments within each stent and in the segment between stents was measured. The diameter narrowing within the closed stent was greater in the high cholesterol group compared with the low cholesterol group: 12 weeks (2.57 +/- 0.09 mm in group I vs 2.14 +/- 0.15 mm in group II, mean +/- S.E., p < 0.05); 16 weeks (2.55 +/- 0.09 mm vs 2.14 +/- 0.12 mm, p < 0.05); 20 weeks (2.59 +/- 0.06 mm vs 1.98 +/- 0.12 mm, p < 0.01); and 24 weeks (2.45 +/- 0.11 mm vs 2.01 +/- 0.11 mm, p < 0.05). No significant differences in the narrowest diameter of the arterial segments were observed between high and low cholesterol groups in the angioplasty alone areas or within the open stents. There was a significant difference in the narrowest diameter between stents with versus those without gaps (at 12, 16, and 20 weeks poststenting in group I and at 4, 8, 12, 16, 20, and 24 weeks in group II). Thus the stent with the least metal is correlated with less stenosis and intimal hyperplasia. From these data we conclude that both stent design and serum cholesterol are important factors for restenosis after stent implantation.
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PMID:Effects of stent design and serum cholesterol level on the restenosis rate in atherosclerotic rabbits. 823 45

We investigated the effect of lead nitrate (0.5-5.0 microM) on the repair of wounded monolayer of cultured bovine aortic endothelial cells. It was morphologically found that lead decreases the appearance of the cells in the wounded area in a concentration-dependent manner without degenerative changes after a 48-h incubation. Although mercury weakly inhibited the repair with nonspecific cell damage, the other cations including bismuth, cobalt, manganese and nickel failed to affect the repair. The inhibition of endothelial repair caused by lead was observed even when stimulated by exogenous either basic or fibroblast growth factor. These results indicated that inhibition of the repair process of damaged endothelial cell layer is a component of lead-induced vascular lesions such as atherosclerosis.
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PMID:Inhibitory effect of lead on the repair of wounded monolayers of cultured vascular endothelial cells. 905 98

We investigated the effect of zinc sulfate on the proliferation of cultured bovine aortic smooth muscle cells stimulated with or without growth factors. Zinc had no effect on the incorporation of [3H]thymidine into the acid-insoluble fraction of the cells stimulated with or without platelet-derived growth factor or transforming growth factor beta 1. However, it was shown that stimulation of the [3H]thymidine incorporation by either basic or acidic fibroblast growth factor was significantly potentiated by zinc. Other cations including copper, manganese and nickel did not exhibit such an activity. The present data suggest that zinc is a particular heavy metal which potentiates vascular smooth muscle cell proliferation stimulated by basic and acidic fibroblast growth factors as well as thrombospondin. Zinc may be involved in the intimal hyperplasia of atherosclerosis.
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PMID:Zinc potentiates the stimulation by basic and acidic fibroblast growth factors on the proliferation of cultured vascular smooth muscle cells. 950 72

Low-voltage-activated T-type Ca2+ channels are present in most excitable tissues including the heart (mainly pacemaker cells), smooth muscle, central and peripheral nervous systems, and endocrine tissues, but also in non-excitable cells, such as osteoblasts, fibroblasts, glial cells, etc. Although they comprise a slightly heterogeneous population, these channels share many defining characteristics: small conductance (< 10 pS), similar Ca2+ and Ba2+ permeabilities, slow deactivation, and a voltage-dependent inactivation rate. In addition, activation at low voltages, rapid inactivation, and blockade by Ni2+ are classical properties of T-type Ca2+ channels, which are less specific. T-type Ca2+ channels are weakly blocked by standard Ca2+ antagonists. Pharmacological blockers are scarce and often lack specificity and/or potency. The physiological modulation of T-type Ca2+ currents is complex: they are enhanced by endothelin-1, angiotensin II (AT1-receptor), ATP, and isoproterenol (cAMP-independent), but are reduced by angiotensin II (AT2-receptor), somatostatin and atrial natriuretic peptide. Norepinephrine enhances these currents in some cells but decreases them in others. T-type Ca2+ currents have many known or suggested physiological and pathophysiological roles in growth (protein synthesis, cell differentiation, and proliferation), neuronal firing regulation, some aspects of genetic hypertension, cardiac hypertrophy, cardiac fibrosis, cardiac rhythm (normal and abnormal), and atherosclerosis. Mibefradil is a new Ca2+ antagonist that is effective in hypertension and angina pectoris. Its favorable pharmacological profile and limited side effects appear to be related to selective block of T-type Ca2+ channels: mibefradil reduces vascular resistance and heart rate without negative inotropy or neurohormonal stimulation, and it also has significant antiproliferative actions.
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PMID:T-type Ca2+ channels and pharmacological blockade: potential pathophysiological relevance. 951 67

The deformability of red blood cells (RBCs) is an important rheologic factor in the maintenance of normal blood flow in the microcirculation. Contrary to the well-known relationship between hyperlipidemia and atherosclerosis, the relationship between RBC rheology and the serum lipid profile has remained controversial and obscure. Moreover, the correlation of high-density lipoprotein (HDL)-cholesterol and RBC deformability has not been fully understood. In the present cross-sectional study of 139 apparently healthy subjects, we investigated whole-cell deformability (filterability) of RBCs in relation to the lipid profile, using a nickel mesh filter with 3.2-microm pores. RBC filterability was independent of gender, age and serum levels of low-density lipoprotein (LDL)-cholesterol. The filterability was significantly proportional to the HDL-cholesterol values (r = 0.382, p < 0.01), whereas it was inversely proportional to the triglyceride levels (r = -0.259, p < 0.01). These findings may provide new insight into the role of HDL-cholesterol not only in preventing atherosclerotic progression but also in improving RBC filterability.
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PMID:Relationship of high-density lipoprotein cholesterol and red blood cell filterability: cross-sectional study of healthy subjects. 1071 15


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