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

In the study was investigated whether the formation of prostanoids is changed in the different regions of aorta or in clotting whole blood in dependence on development of atherosclerosis. For this question New Zealand rabbits were fed for different periods with a cholesterol rich diet (0.5%). At the end of the different dietary periods the animals were killed and the following parameters estimated: blood: levels of total cholesterol, HDLcholesterol, VLDLcholesterol, cholesterol in the beta-migrating lipoprotein fraction, serum lipid peroxides, TXB2 formation capacity of clotting whole blood; aorta: surface of intima covered with fatty streaks, free and esterified cholesterol, triglycerides, collagen, formation of 6-keto-PGF1a and TXB2 by abdominal and thoracic aortas. The lipid parameter demonstrated a relatively strong correlation with the duration of cholesterol rich diet or the macroscopically detectable atherosclerosis, but the prostanoid formation remained unchanged.
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PMID:Influence of a cholesterol rich diet in rabbits on the formation of PGI2 and TXA2. 163 99

A high frequency restriction fragment length polymorphism (RFLP) at the 3'-end of the pigeon pro alpha 2(1) collagen gene was detected using the restriction endonuclease EcoR1. The distribution of this allelic variant was analyzed in DNA isolated from White Carneau pigeons genetically susceptible to the development of spontaneous atherosclerosis. The atherogenic phenotype in individual pigeons was measured by the determination of total cholesterol and cholesterol ester levels in the celiac focus of the thoracic aorta of adult White Carneau pigeons. Aortic wall cholesterol levels correlated with an increase in lesion size. No correlation, however, was observed between allelic variants of the pigeon pro alpha 2(1) collagen gene and the atherogenic phenotype in White Carneau pigeons suggesting lack of linkage between this allelic marker and the genetic susceptibility to spontaneous atherogenesis. This is the first study of its kind in this animal model and serves to provide a basis for the further analysis of co-segregation of RFLPS in candidate genes to this polygenic phenotype.
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PMID:A restriction fragment length polymorphism in the pigeon pro alpha 2(1) collagen gene: lack of an allelic association with an atherogenic phenotype in pigeons genetically susceptible to the development of spontaneous atherosclerosis. 168 10

The key processes responsible for plaque in atherosclerosis are cholesterol accumulation, caused by increased net uptake of atherogenic lipoproteins; cell proliferation and recruitment, caused by mitogenic and chemotactic activity; extracellular matrix expansion and collagen accumulation, caused by increased intimal cell synthesis; and high rates of cell death, caused by increased metabolic needs of tissue in an unfavorable milieu. Cell death is associated with neovascularization, dense fibrosis, and calcification, with the subsequent plaque complications of hemorrhage and thrombosis. An additional functional feature of atherosclerosis, even in prestenotic stages, is severe vasomotor abnormalities, caused in part by endothelial dysfunction. Reversal of atherosclerosis involves interrupting these processes. Calcium antagonists may block specific stages of atherogenesis. Anticalcifying agents (diphosphonates, thiophenes, and metallic ions) inhibit accumulation of connective tissue. Calcium channel blockers reduce endothelial injury and intimal permeability, block proliferation of intimal cells, inhibit lipid accumulation by a number of mechanisms, and reduce exaggerated vasoconstrictor responses. Thus, calcium antagonists may promote regression of lesions beyond what can be achieved by reducing risk factors alone.
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PMID:Regression of atherosclerosis. A role for calcium antagonists. 171 17

We describe here the basic structure of the aorta, the changes with aging and ultrastructural appearance of atherosclerosis of human and animal models. The architecture of the aortic wall is highly organized, for adaptation to changes of blood pressure. The main cells composing the vessel are endothelial cells and smooth muscle cells. They maintain the integrity and homeostasis of the aorta along with the extracellular matrix of collagen fibrils, elastic fibers and glycosaminoglycans. The structural changes with aging and atherogenesis are a compensative or degenerative phenomenon caused by many factors. Three major cells are the endothelial cell, smooth muscle cell and monocyte-derived macrophages (as well as platelets) all of which are involved in atherogenesis. Foam cells in atheromatous lesions are derived from macrophages and smooth muscle cells. Recently, the molecular biological nature and function of these cells and their derived-factors have been thoroughly investigated in cell culture and in experimental animal models caused by a mechanical injury of the endothelium or by a dietary induced hypercholesterolemia. However, the mechanism of the endothelial injury in vivo as well as formation of atheromatous cores of human atherosclerosis is not exactly understood. Some structural and functional changes inherent to the arterial wall during aging may play an important role in initiation or progression of human atherosclerosis.
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PMID:Ultrastructure appearance of atherosclerosis in human and experimentally-induced animal models. 173 74

Scavenger receptors have been implicated in the development of atherosclerosis and other macrophage-associated functions. The structures and processing of type I and type II bovine macrophage scavenger receptors were examined using polyclonal anti-receptor antibodies. Pulse/chase metabolic labeling experiments showed that both types of scavenger receptors expressed in Chinese hamster ovary (CHO) cells behaved as typical cell surface membrane glycoproteins. They were synthesized as endoglycosidase H-sensitive precursors which were converted to endoglycosidase H-resistant mature forms expressed on the cell surface. The reduced precursor and mature forms were doublets on sodium dodecyl sulfate-gel electrophoresis, primarily because of heterogeneous N-glycosylation. The approximate molecular sizes were: type I precursor, 65/63 kDa; type I mature, 82/76 kDa; type II precursor, 57/53 kDa; and type II mature, 72/65 kDa. During post-translational processing, the cysteine-rich C terminus (SRCR domain) of some of the type I receptors was proteolytically removed to form a relatively stable, approximately 69-kDa degradation product. Type II receptors differ from type I receptors in that they do not have SRCR domains and an analogous proteolytic cleavage was not observed. Several experiments provided strong evidence that the Gly-X-Y-repeat domains in the scavenger receptors oligomerize into collagenous triple helices. For example, alpha,alpha'-dipyridyl, an inhibitor of the collagen-modifying enzymes prolyl and lysyl hydroxylases, interfered with both the kinetics and nature of post-translational receptor processing, and both precursor and mature forms of the receptors in intact cells could be cross-linked with difluorodinitrobenzene into reduction-resistant trimers. In intact cells, precursor receptor trimers (type I, 198 kDa; type II, 176 kDa) were assembled in the endoplasmic reticulum by the noncovalent association of monomers and Cys83-disulfide-linked dimers (type I, 129 kDa; type II, 119 kDa). When cells were lysed in the absence of the sulfhydryl trapping agent iodoacetamide, oxidation of the side chain of Cys17 in the cytoplasmic domain leads to the artifactual formation of reduction-sensitive covalently linked trimers. The approximate masses of the mature dimer and trimer forms were 162 and 237 kDa for type I receptors and 147 and 219 kDa for type II receptors. Cys83-disulfide-linked dimer formation was not required for function because mutant receptors (Cys83----Gly83) assembled into trimers of noncovalently associated monomers and exhibited normal receptor activity. Treatment of cells with difluorodinitrobenzene cross-linked some of the receptors into complexes larger than trimers, raising the possibility that the trimers may assemble into higher order oligomers.
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PMID:The type I and type II bovine scavenger receptors expressed in Chinese hamster ovary cells are trimeric proteins with collagenous triple helical domains comprising noncovalently associated monomers and Cys83-disulfide-linked dimers. 174 71

One of the hypotheses trying to explain the process of aging is the idea of glycation of proteins. This reaction, also called the Maillard or browning reaction, may explain age-related symptoms such as cataract, atherosclerosis and modification of collagen-containing tissues. Diabetics, which possess elevated blood sugar levels, show signs of accelerated aging exposing similar complications. The Maillard reaction, which occurs on a large scale in vivo, may play a key role in the initiation of these symptoms.
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PMID:The role of glycation in aging and diabetes mellitus. 174 74

The effects of benazepril hydrochloride (CGS 14824 A, CAS 86541-74-4), a novel angiotensin I converting enzyme inhibitor, on cardiovascular, visceral and renal functions and on hemodynamics, were studied in various experimental animals. Even at a high dose of 100 mg/kg p.o. benazepirl hydrochloride had no influence on the respiration, heart rate and ECG of normotensive anesthetized cats and, except at higher doses, had little effect on the contractile tension of mammalian isolated atrium, ileum, trachea, stomach fundus strips, vas deferens or uterus. Benazepril hydrochloride even at a high dose of 100 mg/kg p.o. had little effect on spontaneous uterine motility, charcoal transportation and gastrointestinal tract motility. In addition, it did not cause gastric irritation, alter the secretion of gastric and biliary juices, and did not affect the tension of the nictitating membrane or the twitch tension of the gastrocnemius muscle in various experimental animals. Benazepril hydrochloride had no effect on the blood glucose and cholesterol levels in alloxan-induced diabetic rats but decreased the triglyceride and total cholesterol levels in normotensive rats at a dose of 30 mg/kg p.o. Benazepril hydrochloride at 3 mg/kg.day s.c. for 10 weeks caused a significant decrease in aortic atherosclerosis without reducing hypercholesterolemia in cholesterol-fed rabbits. Benazepril hydrochloride at a high dose of 100 mg/kg p.o. showed no effect on the urine volume and urinary excretion of electrolytes but decreased PSP excretion in normotensive rats. At a dose of 3 or 10 mg/kg.day p.o. for 4 weeks benazepril hydrochloride inhibited the increase in the excretion of urinary protein in DOCA/salt spontaneously hypertensive rats. It caused hemolysis at concentrations as high as 0.1-1% in rabbits, however, even at a high dose of 100 mg/kg p.o. it did not affect red blood cell fragility in rats, and, except at a high dose of 10(-4) g/ml, showed little effect on the platelet aggregation response induced by collagen or arachidonic acid in rabbits. From these results, benazepril hydrochloride is considered to be a safe and well-tolerated addition to the therapeutic armamentarium of cardiovascular drugs.
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PMID:General pharmacology of the novel angiotensin converting enzyme inhibitor benazepril hydrochloride. Effects on cardiovascular, visceral and renal functions and on hemodynamics. 179 19

We present the case of a 42-year-old male with familial hypercholesterolemia (FH) who had received long-term low-density lipoprotein (LDL)-apheresis before death occurred, presumably from an arrhythmia. He had been treated with double filtration plasmapheresis (DFPP) for 4 years and selective LDL adsorbent plasmapheresis (LAPP) for 2 years and 7 months. During the period of treatment (6 years and 7 months) he had received a total of 129 sessions of LDL-apheresis. Serum total cholesterol of the patient before the treatment was 638 mg/dl and during the treatment, the time-averaged values ranged from 336 mg/dl to 411 mg/dl for the first 4 years (with DFPP) and from 257 mg/dl to 364 mg/dl for the sequential 2 years and 7 months (with LAPP). Coronary angiograms were analysed for 13 segments of the coronary arteries using a digitized processing system. Analysis documented regression by identifying a reduction in percent stenosis from 34% to 20% in the proximal left circumflex artery (LCX), from 78% to 61% in the proximal right coronary artery (RCA), and from 92% to 72% in the middle RCA. In the other 10 segments analysed no significant regression and no progression were observed. The autopsy findings of the step-wise serial sections of the native coronary arteries did not record the formation of new and/or typical atheroma. In addition, a thickened intima, and an eccentric thickened wall lesion rich in collagen fiber were observed, although an accumulation of foam cells in the thickened wall lesions was found in some segments. This observation suggested scarring of the atheromatous plaque. We confirmed that LDL-apheresis performed over a period of 6 years and 7 months induced angiographic regression of coronary atherosclerosis in the patient with FH, and found that most of the atherosclerotic lesions were changed pathologically into sclerotic lesions rich in collagen fiber.
Atherosclerosis 1991 Sep
PMID:Pathological and angiographic regression of coronary atherosclerosis by LDL-apheresis in a patient with familial hypercholesterolemia. 179

Platelets are involved in the progressive pathogenesis of atherosclerosis. It has been shown that there is usually an increase in platelet aggregation between 6 and 9 a.m.; in the present study. in 10 patients suffering from chronic occlusive arterial disease, the impedancemetric method was used to evaluate, in whole blood, platelet aggregation induced by ADP and collagen the day prior to and the day following the evening administration of 300 mg picotamide. Analysis of the data obtained shows, in accordance with the findings of other authors, in increase of platelet aggregation from 6 a.m. to 9 a.m. This increase is suppressed by the evening administration of the anti-aggregant.
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PMID:[Changes in morning platelet aggregation in patients with peripheral obliterating arteriopathy after evening administration of picotamide]. 182 69

The purpose of this study was to compare the relative effect of n-3 fatty acids on plasma lipids and platelet function in normolipemic subjects (n = 8) with plasma Lp(a) levels greater than 30 mg/dl and normolipemic subjects (n = 7) without detectable plasma Lp(a) concentrations. Six weeks of dietary supplementation (3.8 g EPA and 2.9 g DHA/d) significantly reduced (P less than 0.005) plasma TGs in both groups whereas no changes of plasma TC, LDL-C, HDL-C, and Lp(a), respectively, were found. Collagen- or thrombin-stimulated platelet aggregation and collagen- or thrombin-induced TXB2 generation from platelets decreased by approx. 45% in Lp(a)-negative and Lp(a)-positive platelet donors after a 6 week dietary intake. Four more weeks without n-3 supplementation restored the pretreatment values of TGs, platelet aggregability and TXB2 release. The biophysical properties of platelets from normolipemics with and without high plasma Lp(a) concentrations revealed a similar structural order of platelets at 37 degrees C using DPH, TMA-DPH, or 6-AS as fluorescent probes. Also similar temperature-dependent changes in platelet fluidity from 37 degrees C to 17 degrees C were observed in platelet preparations from Lp(a)-positive and Lp(a)-negative subjects. However, no subtle changes in the structural order of platelets due to nutrient intakes were found in all subjects (n = 15, 19-28 yrs) using fluorescence polarization technique. The present data suggest a similar in vitro platelet behaviour from normolipemic subjects with and without high plasma levels of Lp(a) (which is considered a risk for premature atherosclerosis) in contrast to platelet aggregability and platelet fluidity in certain hyperlipidemic stages.
Atherosclerosis 1991 Jun
PMID:Effects of dietary fish oil supplementation on platelet aggregability and platelet membrane fluidity in normolipemic subjects with and without high plasma Lp(a) concentrations. 183 37


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