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

Arteriosclerosis is caused by many factors. These pathogenic factors especially over-nutrition, nicotinabusus, deficiency of muscular exercise, muscular overstrain, emotional stress and concomitant basic diseases, especially arterial hypertension, diabetes mellitus and dyslipidemia are the most important points for preventive and therapeutical action. When possible the risk factors has to be eliminated, arterial hypertension, diabetes mellitus and dyslipidemia have to be treated orderly. In the pathogenesis of arteriosclerosis and atherosclerosis are known disturbances of the lipid metabolism, the blood coagulation and the metabolism of the arterial wall cells most important. Application of anticoagulants and lipid lowering medicaments did not come up to our expectations. Experiences with animal models and a double blind study (secondary prevention of myocardial infarction) have given good reason for recommending antirheumatic or as we like to say, mesenchyme suppressive drugs.
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PMID:[Prevention and therapy of arteriosclerosis (author's transl)]. 3 60

This study was carried out to determine the evolution of atherosclerotic lesions during a therapeutic period during which regression might be appreciated. We produced aortic and coronary atherosclerosis in 27 young adult stumptail macaques (Macaca arctoides) by feeding a diet supplemented with 2% cholesterol and 25% fat. Hypertension was produced by bilateral or unilateral narrowing of the renal artery. After six months of this regimen, four monkeys were killed (group 1) and 23 monkeys were divided into three groups: group 2 received unsupplemented diet; group 3 received the same diet as group 2 and drug treatment for hypertension; group 4 was continued on the atherogenic diet and received antihypertensive drug treatment. The results indicate that deleting the atherogenic diet leads to a decrease in the lipid content of the lesions and a transformation of the lipid laden atherosclerotic plaques into lipid-poor, fibro-collagenous lesions, with a decrease in the amount of coronary luminal narrowing. Partial control of systolic hypertension by antihypertensive drugs did not accelerate the involution of the atherosclerotic lesions over the relatively short period of this study. No statistically significant correlation by regression analysis was observed between the level of blood pressure elevation, the plasma renin activity, or the degree of the drug response, and the severity and extent of the atherosclerotic lesions. Furthermore, severe arterial hypertension without an atherogenic diet (group 5) produced arteriosclerosis of the aorta, and intensified branch cushions in the coronary arteries, without inducing lipid deposition in either vascular bed.
Atherosclerosis 1978 Apr
PMID:Diet-induced atherosclerosis and experimental hypertension in stumptail macaques (Macaca arctoides). Effects of antihypertensive drugs and a non-atherogenic diet in the evolution of lesions. 9 44

The aortic content of glycosaminoglycans and collagen as well as the uptake of [125 I] albumin were studied in 53 male albino rabbits during hair-shedding and outside the period of hair-shedding to elucidate the previously reported resistance to experimental arteriosclerosis during the shedding period [1]. The concentration of hyaluronic acid was highest during hair shedding, decreasing towards the non-shedding period. The content of dermatan sulphate, chondroitin-4, 6-sulphate and hydroxyproline was lowest during sheeding and highest outside the sheeding period. Accordingly, the incorportation of [35 S] sulphate in chondroitin -4, 6-sulphate and the dermatan plus heparan sulphate fraction was increased outside shedding, consistent with a stimulated synthesis. The concentration of hyaluronic acid was negatively correlated to the uptake of [125I] albumin, and the dermatan sulphate content was positively correlated to the content of hydroxyproline. The higher concentration of hyaluronic acid during the period of shedding may improve the elastic properties as well as the ability of the aortic wall to absorbe the haemodynamic strain involved in the vascular injury of this type of experimental arteriosclerosis [2]. The decrease in the concentration of hyaluronic acid simultaneously with an increase in the aortic content of collagen as well as of chondroitin-4, 6-sulphate and dermatan sulphate may imply a greater stiffness of the aorta resulting in a higher susceptibility to injury. The relationship between hyaluronic acid and [125 I] albumin is consistent with an importance of hyaluronic acid to the susceptibility of the arterial wall to deposition of macromolecules such as the lipids. Our observations represent an example of endogenous conditioned variations in the aortic content of glycosaminoglycans and hydroxyproline accompanied by a variation in the susceptibility to experimental arteriosclerosis.
Atherosclerosis
PMID:Seasonal variations in the susceptibility of the aortic wall to atherosclerosis. Biochemical studies of glycosaminoglycans and collagen of rabbit atherosclerosis. 13 91

Acid extracts were made of the pituitary glands of non-arteriosclerotic male and female virgin rats and arteriosclerotic, male and female breeder rats. The ACTH content of these pituitary glands was determined by measuring the amount of corticosterone produced by the adrenal glands of healthy but hypophysectomized rats when challenged by the various ACTH acid extracts. The pituitary glands of the arteriosclerotic animals were significantly heavier than non-arteriosclerotic rats and contained decreased amounts of ACTH commensurate with the severity of the pituitary donor's arteriosclerosis. Similarly, arteriosclerotic donors had heavier adrenal glands but contained considerably less corticosterone than non-arteriosclerotic virgin rats. Male breeder rats developed microscopic aortic lesions involving intimal mesenchymal cell and ground substance alterations whereas the female breeder lesions progressed from intimal ground substance and connective tissue changes to medial elastolytic degeneration and eventual medial cartilaginous and osseous metaplasia. Histopathologic examination of the pituitary and adrenal glands demonstrated hyperplasia of basophil and other cytologic elements of the pituitary gland including colloid-filled cysts and lipid depletion of the zona glomerulosa as well as hemorrhage and thrombosis of the adrenal cortex of the arteriosclerotic breeder rats. The hypothesis is made that repeated breeding leads to abnormal hypothalamic regulation of pituitary gland synthesis and release of ACTH, which, in turn, contributes to abnormal adrenal glandular function conditioning the aortic wall toward abnormal changes in mesenchymal cell activity and metabolism of connective tissue ground substance.
Atherosclerosis
PMID:ACTH content of pituitary glands of arteriosclerotic breeder vs. non-arteriosclerotic virgin rats. 17 94

There is a growing number of lipoprotein markers recognized by immunological, electrophoretic, and other biochemical methods, and a beginning has been made on studying their modes of inheritance and linkage relations. Suggestive but inconclusive evidence of a relation between the cerumen polymorphism and arteriosclerosis has been published. Associations of the ABO blood groups with cardiovascular disease and serum lipid levels have been established, but the exact relation to lipoproteins and atherosclerosis remains to be determined.
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PMID:Genetic markers in atherosclerosis: a review. 18 Feb 92

Increased aortic and liver prolyl hydroxylase activity has been suggested as an early biochemical indicator of the fibrotic changes which occur in rabbits with injury induced arteriosclerosis. Daily administration of epinephrine (0.025-0.050 mg/kg, i.v.) and thyroxine (0.050 mg/kg, i.p.) to rabbits for 3 weeks produced aortic fibrous plaques with a 4-fold increase in aortic prolyl hydroxylase and also a 5-fold increase in liver prolyl hydroxylase. Histopathologically, the livers of these rabbits show subcapsular areas of necrosis. When total prolyl hydroxylase related antigen was measured. the increase in liver prolyl hydroxylase activity accounted for only a small portion of the total prolyl hydroxylase antigen. However, in the aorta a majority of the increase in antigen is due to the increased amount of enzyme. DNA content per aorta was unchanged and RNA content increased in the aortic tissue of the arteriosclerotic rabbits. However DNA and RNA levels increased 60% in the livers of arteriosclerotic rabbits. In vitro incorporation of radioactively labeled proline into collagenase digestable protein was at least 2-fold greater in aorta and liver minces from arteriosclerotic rabbits. Michaelis--Menten kinetic parameters were obtained for the liver prolyl hydroxylase purified by affinity chromatography from arteriosclerotic rabbits. The Km for the enzyme from treated animals was not significantly different from control. However, the Vmax of the enzyme purified from diseased liver was 4-fold greater when compared to controls.
Atherosclerosis 1976 Sep
PMID:Increased collagen synthesis and the kinetic characteristics of prolyl hydroxylase in tissues of rabbits with experimental arteriosclerosis. 18

Of four groups of chickens, two (groups I and II) were infected with MDV and two were not (groups III and IV). Groups I and III were fed diets low in lipid, and groups II and IV were fed cholesterol-supplemented diets. Striking grossly visible atherosclerotic lesions were seen in large coronary arteries, aortas, and major aortic branches of infected normocholesterolemic and hypercholesterolemic chickens (groups I and II). In contrast, grossly visible atherosclerotic lesions were not seen in uninfected normocholesterolemic chickens (group III), nor in uninfected hypercholesterolemic chickens (group IV). Microscopically, arterial changes in the infected animals were characterized by occlusive fibromuscular intimal thickening which formed fibrous caps overlying areas of atheromatous change. This change closely resembled chronic atherosclerosis in man. These results may have important bearing on our understanding of the etiology and pathogenesis of human arteriosclerosis since there is widespread and persistent infection of human populations with up to five different herpes-viruses.
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PMID:Virus-induced atherosclerosis. 20 24

Imbalancing nutritionally adequate diets with an excessive amount of fat calories and cholesterol has obscured the fact that intimal thickening occurs spontaneously in time on low-fat cholesterol-free diets during the aging process, and that intimal thickening can be accelerated by dietary angiotoxic "risk factors." Electron microscopy of arterial tissue from animal models identified degenerated smooth muscle cells in the fetus from sows kept on low-fat cholesterol-free diets. After birth, the degenerated smooth muscle cells increased in number with age. The presence of angiotoxic "risk factors" such as oxidized cholesterol and vitamin D3 (cholecalciferol) in the diet of such animal models increased the frequency of smooth muscle cell death in their arteries. Two types of pathology could be developed in the thoracic aorta by continuous or short term feeding of 12.5 times more vitamin D than normally present in commercial rations: 1) a diffuse fibroelastic intimal thickening in the thoracic aorta (arteriosclerosis) with no evidence of lipid deposition by continuous feeding of vitamin D or 2) an initimal thickening in the thoracic aorta and intimal thickening with foam cells and extracellular lipid deposits (atherosclerosis) in the coronary arteries after a short period of supplemental vitamin D followed by 3 to 4 months of supplement-free diets. These two types of arterial damage were identical to that in the plugs of thoracic aorta obtained as a by-product of elective coronary bypass surgery. Although all of the possible sources of oxidized cholesterol in the diet have as yet not been identified, laboratory studies have identified oxidized cholesterol as an angiotoxic factor. Since population groups that consume less vitamin D-supplemented foods, less deep fat fried cholesterol-containing foods, and less hydrogenated fats have a lower incidence of coronary heart disease than Americans, it seems judicious for food processors to reduce these previously unconsidered risk factors to a minimum. This could be done by eliminating vitamin D2 and D3 from all vitamin supplements, from all food and cereal products and from the diet of livestock 1 month before they were killed so that the intake of vitamin D is no larger than the 400 IU/quart in milk which is necessary to prevent rickets in children. Deep fat fryers, which are kept at almost 200 C for 24 hr/day, could perhaps be replaced with microwave ovens in fast food chain outlets. Processors could hydrogenate vegetable oils to a minimum trans fatty acid content and rearrange this fat with polyunsaturated fats to produce high polyunsaturated fats trans-free margarines and shortenings.
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PMID:Nutrition imbalance and angiotoxins as dietary risk factors in coronary heart disease. 21 61

The proliferation of aortic smooth muscle cells (ASMC) of Wistar rats, impaired by risk factors such as arterial hypertension, diabetes mellitus, atherogenic diet and staphylolysin injections and of normal Wistar rats treated with antirheumatic drugs such as prednisolone and acetylsalicylic acid was investigated. The cells of these animals were cultivated, subcultivated, and in the 2nd subcultures the cell numbers/5 ml medium were counted by means of Coulter Counter, and the cells were incubated with [3H]thymidine and the percentage of labelling in 100 or 1000 counted cells was stated. The effect of risk factors such as LDL and staphylolysin and of antirheumatic drugs such as prednisolone, acetylsalicylic acid, D-penicillamine and chloroquine added to the 2nd subcultures of cultivated ASMC of normal minipigs was investigated by the same method. The proliferation of cultivated ASMC of rats impaired by risk factors was accelerated. The proliferation of cultivated ASMC of rats treated with antirheumatic drugs was inhibited. The proliferation of ASMC of minipigs in the 2nd subcultures was activated by addition of risk factors and inhibited by addition of antirheumatic drugs. Antirheumatic drugs given to the rats and added to the medium of the 2nd subcultures of ASMC of normal minipigs inhibit the acceleration of ASMC proliferation induced by simultaneously given risk factors. The proposal to augment up our arsenal of the hitherto existing preventive and therapeutical measures by the application of antirheumatic drugs based on the experimental models referred to is supported by the result of a limited prospective double-blind-study of a sample of 133 male patients after myocardial infarction. The most remarkable result that the acceleration of the ASMC proliferation, the real pathologic process of arteriosclerosis, is inhibited by the application of antirheumatic drugs, at exactly the same time as the acceleration of the fibroblast proliferation, the real pathologic process in rheumatic diseases--ASMC and fibroblast, both being mesenchymal cells--recommends the use of these drugs in the prevention and therapy of human arteriosclerosis. The surprising result of our in-vivo experiments, that the acceleration of the growth of the ASMC induced by risk factors and the inhibition of the growth induced by antirheumatic drugs persist in the subcultures, is explained by the "selection theory" that there are dissimilar kinds of ASMC in normal arteries and that they react differently.
Atherosclerosis 1979 Oct
PMID:Effect of risk factors and antirheumatic drugs on the proliferation of aortic wall cells. 22 70

The extreme variations with which atherosclerotic disease presents as regards progression index, arterial bed localization frequency, malignity and invasiveness in different ages and often as regards different anatomopathological aspects characterizing the formation and course of the primary lesion, mean that there are still many unknowns in the aetiopathogenesis, diagnosis and operative indications for this disease. Such problems are more and more important to the vascular surgeon who, with the development of atherosclerotic disease, sees the long-term results of his arterial reconstructive surgery compromised. The vascular surgeon is therefore directly involved with his colleagues in the internal medicine and pharmacological departments in problems connected with the pathogenesis of arteriosclerosis, and indeed he contributes to setting new constraints on the choice of prosthetic materials, for use in cases of bridge-work, and in the creation of new surfaces by means of thrombendarteriectomy. On the basis of such considerations, the IInd Surgical Clinic of Milan University began, in 1975, a study whose end purpose was the drafting of a clinical card designed for data computerization. Compiled by the surgeon, it is intended essentially for vascular surgeons. However, as it is personally considered that by the very nature of the disease, the atherosclerosis approach must be interdisciplinary, it also concerns physicians in the internal medicine, pharmacological and dietological departments.
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PMID:[The SITAR Project. A new approach to diagnosis and surgical indication in arteriopathic patients]. 32 30


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