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

Cardiovascular disease is a major cause of morbidity and mortality in the U.K. and other developed countries. In the U.K., mortality from coronary heart disease has increased progressively over the past 25 years, particularly in males. This paper examines the possible role of trace metals in the development of cardiovascular disease, with particular reference to the effects of cobalt, cadmium and lead in myocardial disease, atherosclerosis and hypertension. It is concluded that cobalt is an unimportant factor in community levels of cardiovascular disease, that cadmium has striking effects on blood pressure in animals and that there is some evidence for an association between environmental lead and high blood pressure.
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PMID:Cardiovascular disease and trace metals. 4 Feb 34

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

Initial and Co-35-induced parameters of lipid metabolism and hemostasis were studied in rabbits with experimental atherosclerosis. Control atherosclerotic animals were administered cobalt chloride and placebo. The findings demonstrated initially increased levels of cholesterol, lecithin, beta-lipoproteins, lysolecithin, sphingomyelin, cephalin, saturated acids in low levels of phosphatidylserine, polyglycerophosphatide and unsaturated acids. Hemostasis was characterized by hypercoagulation. A course of Co-35 brought about positive shifts in both lipid metabolism and hemostasis. Co-35 is recommended as an effective means against atherosclerosis.
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PMID:[Experimental atherosclerosis and its correction with Co-35]. 147 48

A wide-range complex of biochemical techniques was used to study metabolic processes in workers exposed to cobalt and ethanol. In practically healthy workers were found laboratory manifestations of hepato-biliary irritations, hyperpermeability of the hepatocytes' cytoplasmic membrane, cholestasis syndrome, initial manifestations of muscular dystrophy and minor signs of atherosclerosis risks. The biochemical shifts were like those in alcoholism cases. It was suggested that, under the existing technological conditions of cobalt-containing hard-facing alloys' powder processing, the action of ethanol increased the toxic effect of cobalt.
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PMID:[Metabolic status in workers engaged in the production of cobalt-containing powder compositions of hard alloys]. 179 96

The properties of CDP-choline:1,2-diacylglycerol cholinephosphotransferase (CPT) (EC 2.7.8.2.), which catalyzes de novo synthesis of phosphatidylcholine, were studied in rat arterial wall. The optimal pH of CPT of the arterial wall was about 8.5. On subcellular fractionation of the arterial wall, the highest activity was found in the microsome-rich fraction; the cytosolic fraction showed only a trace of activity. The Michaelis constant (KM) for CDP-choline was 0.019 mM. The CPT activity of a homogenate of arterial wall increased linearly with increase in concentration of diolein up to 3.2 mM. 20 mM magnesium and 0.2 mM manganese ions caused marked activation respectively and essential for the activity. Calcium, barium, cobalt, copper, and ferrous ions were inhibitory. 0.5 mM ethylenediaminetetraacetic acid (EDTA) and 0.5 mM glycoletherdiamine-N,N,N'N'-tetraacetic acid (GEDTA) increased the activity in the presence of 10 mM magnesium ion. Sonication of the enzyme solution and addition of high concentration of detergent, such as Triton X-100 and Tween 20, markedly decreased the activity. Porcine liver phosphatidylcholine, phosphatidylethanolamine, and especially polyenephosphatidylcholine increased CPT activity of the arterial wall, while lysophosphatidylcholine was strongly inhibitory. The properties of arterial CPT activity under various conditions are discussed.
Atherosclerosis 1982 Jun
PMID:Studies on CDP-choline:1,2-diacylglycerol cholinephosphotransferase activity in rat arterial wall. 628 57

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

The role of some so-called primary and secondary (or oligo-elements) elements in the physiopathology of the cardiocirculatory system has been well known from a number of years and they have been regularly included in the treatment protocols. Some, including K, Ca, Mg and Zn, are extremely well known and widely used in clinical practice. Recently, however, a growing number of studies have focused on the biological importance of other oligo-elements in the pathogenetic mechanisms of atherogenesis and its clinical manifestations. This study aimed to verify the exact role of free cobalt in the physiopathology of the chronic obstructive arterial diseases (COAD). A total of 80 patients affected by 2nd stage COAD were examined and the levels of some oligo-elements, including Co, were assayed. Constantly low levels were found (85% of cases) in relation to other oligo-elements studied (Cu, Zn, Mg, Ca). This findings is particularly interesting since it confirms the biochemical hypothesis of atherosclerosis according to which parietal damage plays a central role in the pathogenetic mechanism. Some enzymatic deficiencies, which lead to changes in membrane stability at the level of the endothelial cells, are closely related to the presence of tissutal and humoral peroxidation products. These peroxides (lipid peroxides), which are formed following the interaction of fatty acids with oxygen free radicals, have been identified by a number of studies as being responsible for endothelial damage. Several authors have shown that lipid peroxidation is involved in the atherogenic process through several mechanisms entailing monocytic activity and reduced prostacyclin (PG2) synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hypocobaltemia in chronic obstructive arteriopathy. Physiopathologic and therapeutic importance]. 847 50

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

Evident disparities in relationships make it desirable to consider several disorders separately. (1) Alcoholic cardiomyopathy was perceived 150 years ago, but understanding was clouded by recognition of beriberi and of synergistic toxicity from alcohol with arsenic or cobalt. (2) A report of a link between heavy drinking and hypertension in WWI French soldiers was apparently ignored for > 50 years. Epidemiological and intervention studies have now firmly established this association, but a mechanism remains elusive. (3) The 'holiday heart syndrome', an increased risk of supraventricular tachyarrhythmias in alcoholics, has been widely known to clinicians for 25 years; data remain sparse about the total role of heavier drinking in cardiac rhythm disturbances. (4) Failure of earlier studies to distinguish types of stroke impeded understanding; it now seems probable that alcohol drinking increases risk of haemorrhagic stroke but lowers risk of ischaemic stroke. (5) Heberden reported angina relief by alcohol in 1786, and an inverse alcohol-atherosclerosis association was observed by pathologists early in this century. Recent population studies and plausible mechanisms support a protective effect of alcohol against coronary disease. International comparisons dating back to 1819 suggest beverage choice as a factor, but this issue (the 'French Paradox') remains unresolved.
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PMID:Alcohol and cardiovascular diseases: a historical overview. 994 84

Exposure to metals may promote atherosclerosis. Blood cadmium and lead were associated with peripheral arterial disease (PAD) in the 1999-2000 National Health and Nutrition Examination Survey (NHANES). In the present study we evaluated the association between urinary levels of cadmium, lead, barium, cobalt, cesium, molybdenum, antimony, thallium, and tungsten with PAD in a cross-sectional analysis of 790 participants > or =40 years of age in NHANES 1999-2000. PAD was defined as a blood pressure ankle brachial index < 0.9 in at least one leg. Metals were measured in casual (spot) urine specimens by inductively coupled plasma-mass spectrometry. After multivariable adjustment, subjects with PAD had 36% higher levels of cadmium in urine and 49% higher levels of tungsten compared with noncases. The adjusted odds ratio for PAD comparing the 75th to the 25th percentile of the cadmium distribution was 3.05 [95% confidence interval (CI), 0.97 to 9.58]; that for tungsten was 2.25 (95% CI, 0.97 to 5.24). PAD risk increased sharply at low levels of antimony and remained elevated beyond 0.1 microg/L. PAD was not associated with other metals. In conclusion, urinary cadmium, tungsten, and possibly antimony were associated with PAD in a representative sample of the U.S. population. For cadmium, these results strengthen previous findings using blood cadmium as a biomarker, and they support its role in atherosclerosis. For tungsten and antimony, these results need to be interpreted cautiously in the context of an exploratory analysis but deserve further study. Other metals in urine were not associated with PAD at the levels found in the general population.
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PMID:Metals in urine and peripheral arterial disease. 1607 51


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