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

The physician who understands the pathophysiology of angina pectoris can apply rational therapeutic measures based on an appreciation of the determinants of myocardial oxygen supply and demand. Most patients with angina secondary to coronary atherosclerosis can be treated conservatively using a systematic approach that includes correction or removal of underlying causes or precipitating factors and the judicious use of sublingual nitroglycerin. In patients with more resistant angina, use of oral or topical nitroglycerin or sublingual isosorbide dinitrite as well as propranolol can be advised. Aortocoronary bypass surgery can offer significant improvement in carefully selected patients with frequent angina poorly controlled by medical therapy. The most important consideration in the treatment of angina is protection of coronary blood flow reserve by primary prevention of the atherosclerotic process itself. All individuals from families prone to coronary artery disease should be evaluated for alterable risk factors, the most important being cigarette smoking, hypertension, and hypercholesterolemia. Considering the high risk of unheralded sudden death in previously asymptomatic patients with coronary atherosclerosis, angina can, in a sense, be considered a fortunate harbinger of coronary stenosis, identifying candidates for secondary preventive measures aimed at retarding the progression of vascular disease. More importantly, angina serves as an index for detecting families at high risk of coronary artery disease, in whom early application of primary prevention may afford a more promising outlook.
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PMID:Angina pectoris. Diagnosis and treatment. 0 83

Eleven substances capable of either augmenting or depleting the alpha- and - beta-adrenergic capacities of the autonomic nervous system were administered to rats exhibiting hypothalamic hypercholesterolemia and to normal controls. Only the beta-adrenergic blocking agents propranolol and possibly 6-OH dopamine were observed to alter (raise) the serum cholesterol concentration, and this occurred in both experimental and control animals. Neither atropine, nor the serotonin-depleting agent, rho-chlorophenylalanine, nor the serotonin-antagonist cyproheptadine, were observed to alter serum cholesterol level. Such absence of effect was also noted with metaraminol, phenoxybenzamine, isoproterenol, epinephrine, reserpine, and alpha-methyl tyrosine.
Atherosclerosis
PMID:Neurogenic hypercholesterolemia: influence of autonomic drugs. 0 62

The body cholesterol pool increases with decreasing plasma-high-density-lipoprotein (H.D.L.) but is unrelated to the plasma concentrations of total cholesterol and other lipoproteins. This finding supports existing evidence that H.D.L. facilitates the uptake of cholesterol from peripheral tissues and its transport to the liver for catabolism and excretion. Plasma-H.D.L., is reduced in several conditions associated with an increased risk of future ischaemic heart-disease (I.H.D.), namely hypercholesterolaemia, hypertriglyceridaimia, male sex, obesity, and diabetes mellitus, while subjects with existing clinical I.H.D. have lower levels of H.D.L. than healthy subjects within the same community. It is proposed that a reduction of plasma-H.D.L. concentration may accelerate the development of atherosclerosis, and hence I.H.D., by impairing the clearance of cholesterol from the arterial wall.
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PMID:Plasma-high-density-lipoprotein concentration and development of ischaemic heart-disease. 4 38

The experiments were conducted in 14 male rabbits dynamically on the 5th, 10th, 20th, 30th, 40th, 60th and 80th day of the central nervous system tension or at rest, including the studies of lipid metabolism (total cholesterol and beta-lipoproteins content), the function of the thyroid gland (protein bound iodine content) and the function of the adrenal cortex (11-OCS content). Such lasting stimulation of the adrenal cortex was found to be accompanied by hypercholesterolemia, hyper-beta-lipoproteinemia, elevated 11-OCS level and lack of thyroid function changes. A lasting tension of the central nervous system against the background of chronic stimulation of the adrenals delays the development of hypercholesterolemia and hyper-beta-lipoproteinemia, reduces the function of the thyroid gland, and increases the function of the adrenal cortex. The observed shifts in the lipid metabolism may be of atherogenic importance. The obtained data may be useful for the study of the pathogenesis of hormonal shifts in atherosclerosis.
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PMID:[Indices of lipid metabolism, thyroid gland and adrenal cortical function in prolonged stress of the central nervous system in chronic stimulation of the adrenals]. 6 38

Transfer of low-density lipoprotein (L.D.L.2) from plasma to arterial intima was studied in 16 patients undergoing arterial surgery. Autologous labelled lipoprotein was used to demonstrate that L.D.L.2 enters the intima from plasma. Net flux of L.D.L.2 appeared to increase with age. Within each age-group the net flux of L.D.L.2 showed a pronounced positive correlation with plasma-L.D.L.-cholesterol concentrations. This may account in part for the association between hypercholesterolaemia and the development of atherosclerosis.
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PMID:Influence of lipid concentrations and age on transfer of plasma lipoprotein into human arterial intima. 7 Jun 86

The morphology of endothelial cells during the induction of atherosclerosis in the descending aortic arch of the hypercholesterol rabbit was studied in situ by scanning electron microscopy (SEM) following silver staining, fixation at physiological pressure, and air-drying of specimens- The earliest deviations from normal endothelial morphology were observed 3 weeks after starting to feed a semi-synthetic diet containing 20% beef fat and 0.2% cholesterol. These were (1) the occurrence of brightly silver stained (argyrophilic) cells, (2) areas of irregularly shaped cells which were often larger and more weakly stained than normal cells and (3) increased incidence of stigmata and stomata associated with the irregular cells. After 6 weeks of hypercholesterolaemia, similar changes were present in the endothelium, but were often also associated with sub-endothelial swelling. These represented the first atherosclerotic lesions. Following 12, 20 and 24 weeks of hypercholesterolaemia, larger raised macroscopic lesions were observed which were always endothelialized. Endothelial morphology and lesion topography suggested that early fatty streaks were composed of numerous focal swellings. In addition to the abnormal endothelial morphology noted at 6 weeks, endothelial cells overlying more advanced lesions became rounded in outline.
Atherosclerosis 1977 Jun
PMID:Aortic endothelial cell morphology observed in situ by scanning electron microscopy during atherogenesis in the rabbit. 7 Nov 55

Detected using a method involving gradient electrophoresis on polyacrylamide gel, the presence of a high level of an Lp(a) was demonstrated in 17% of control subjects and 39% oh hyperlipidaemic subjects explored. The difference appeared to be particularly significant in subjects with a pure hypercholesterolaemia (type IIA) or dominant hypercholesterolaemia (type IIB), which may be accounted for by the antigenic communities and related substances in the lipid composition uniting Lp(a) to LDL. The association of frank atherosclerosis with the hyperlipidaemia substantially increased the frequency of high levels of circulating Lp(a). A combined elevation of levels of Lp(a) and LDL would seem to be associated with a particular atherogenic power.
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PMID:[Detection of a new lipoprotein: Lp(a). Its occurrence in atherosclerosis with or without hyperlipemia]. 7 59

Sarcoplasmic reticulum (SR) fragments from the skeletal muscles of rabbit with marked atherosclerosis possessed decreased Ca2+-accumulating capacity. Lowering of transport efficiency, namely reduction of the Ca/ATP ratio from 1.9--normal value--to 0.9 during the experiment at 26 degrees C was accompanied by activation of Ca-ATPase and simultaneously of the rate of Ca2+ outflux from the SR. Arrhenius plots of Ca-ATPase temperature dependence characterized under normal conditions by a break at 20--21 degrees C was linearized under hypercholesterolemia. At the same time there was a rise (from 0.03 under normal conditions to 0.15 in atherosclerosis) of cholesterol/protein ratio in the SR membrane preparations. Activation energy for Ca-ATPase crude membranes under normal conditions was equal to 15.6 and 28.7 kcal/mol above and below the break point respectively; this value for Ca-ATPase of membranes with increased cholesterol level was 19 kcal/mol for all the temperatures investigated.
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PMID:[Several properties of the Ca-pump of rabbit skeletal muscle sarcoplasmic reticulum in hypercholesteremia]. 15 Feb 94

It is possible to establish atherosclerosis in rabbits by feeding semi-synthetic diets that are high in carbohydrate and saturated fat and devoid of cholesterol. Addition of saturated fat to laboratory chow does not render the chow atherogenic. When rabbits were fed diets which differ only in the carbohydrate component, starch was found to be more atherogenic than sucrose which, in turn, was more atherogenic than glucose. All the diets were hypercholesteremic and hypertriglyceridemic. In another series of experiments diets containing fructose or sucrose were more atherogenic than diets containing glucose, lactose or sorbitol. Baboons were feed semi-synthetic diets containing fructose, sucrose, starch or glucose (but no cholesterol) for one year. Serum cholesterol levels were 155-165 mg/dl in all test groups. The normal baboon cholesterol level is 115 mg/dl. Serum triglycerides were elevated from the normal level of 73 mg/dl to about 110 mg/dl in the groups fed starch and glucose and to about 125 mg/dl in the groups fed fructose and sucrose. Liver and lung cholesterol ester levels were also raised. The test groups all showed aortic sudanophilia. The most severe sudanophilia was observed in the fructose group (11.2% of surface area) and the least in the glucose group (6.2% of surface area). The biliary cholesterol specific activities (after administration of (3-H)-melvalonic acid) were the same in all groups, but biliary bile acid specific activity was higher in the control baboons than in test animals. These data, plus the higher primary/secondary bile acid ratio observed in the test animals, suggest that reduced bile acid synthesis may be one cause of the hypercholesteremia observed in animals fed the semi-synthetic diets.
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PMID:The effects of feeding various carbohydrates on the development of hypercholesterolemia and atherosclerosis. 16 59

Cholesterol feeding in miniature swine resulted in a hypercholesterolemia with a distinctive hyperlipoproteinemia and the subsequent development of atherosclerosis. Alterations in the type and distribution of plasma lipoproteins induced by cholesterol feeding were as follows: (a) the occurrence of beta-migrating lipoproteins (B-VLDL) as well as very low density lipoproteins in the d less than 1.006 ultracentrifugal fraction; (b) an increased prominence of the intermediate lipoproteins (d = 1.006-1.02); (c) an increased prominence of low density lipoproteins; and (d) the occurrence of a distinctive lipoprotein with alpha mobility which was referred to as HDLc (cholesterol induced). Characterization of the various plasma lipoproteins included chemical composition, size by electron microscopy, and apoprotein content. The B-VLDL resembled the beta-migrating lipoproteins of human Type III hyperlipoproteinemia and contained a prominent protein equivalent to the arginine-rich apoprotein in addition to the B apoprotein, apo-A-I, and the fast-migrating apoproteins (apo-C). The HDLc were rich in cholesterol, ranged in size from 100 to 240 A in diameter, and contained the arginine-rich apoprotein and apo-A0I but lacked the B apoprotein. The arginine-rich apoproteins isolated from B-VLDL and HDLc by gel chromatography were similar in amino acid analyses, with glutamic acid as their amino-terminal residue. The occurrence of a spectrum of cholesterol-rich lipoproteins which contained the arginine-rich apoprotein with the occurrence of accelerated atherosclerosis suggested an interesting, although speculative, association.
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PMID:Swine lipoproteins and atherosclerosis. Changes in the plasma lipoproteins and apoproteins induced by cholesterol feeding. 16 8


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