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 influence of abdominal aortic stenosis on the uptake of the protein-binding trypan blue dye and 131I human serum albumin (HSA) has been studied. The major change was a region of high uptake proximal to the stenosis, returning to normal by the level of the renal arteries. There was reduced uptake distal to the stenosis, apart from occasional small areas of high uptake probably due to turbulence. The increase in uptake immediately proximal to the stenosis was dependent on the severity and duration of the stenosis. Removal of the stenosis immediately before the injection of dye and 131I-HSA still resulted in elevated uptake in the proximal region. Some haemodynamic modifications resulting from a stenosis are described. It is suggested that the most satisfactory haemodynamic explanation of the observed uptake change is a proximal increase in oscillatory pressure/strain. The relevance of these findings to atherosclerotic development at and above arterial junctions is discussed.
Atherosclerosis 1977 Feb
PMID:Influence of experimental stenosis on uptake of albumin by the abdominal aorta. 83 55

The uptake of trypan blue and [131I]human serum albumin (HSA) has been studied in the dog's abdominal aorta between 1 and 42 days after removal of an experimental stenosis (approximately 90%) applied 1 week previously. Previous work has shown that when the stenosis was present during circulation of these markers, their uptake was increased immediately proximal to the stenosis decreasing to normal by the renal artery level. Distal to the stenosis uptake was reduced apart from small areas of high uptake probably due to turbulent jet impacts. Within the stenosed section the uptake was normal. In this present study it was found that, after removal of the stenosis, proximal uptake initially remained elevated, returning to normal after approximately 15 days whilst the distal uptake returned to normal after approximately 10 days. In the previously stenosed section uptake was increased markedly following the release of the stenosis but returned to normal within approximately 20 days. The relationship of these findings to alterations in the local haemodynamic state and to possible changes in endothelial morphology are discussed.
Atherosclerosis 1977 Oct
PMID:Time dependence of [131I]albumin uptake following removal of an experimental aortic stenosis. 91 73

Antibodies to erythrocytes of sheep and human serum albumin were formed in rabbits with alimentary atherosclerosis as intensively as in control. Trasilol failed to affect the antibody formation in normal animals, but sharply decreased the production of specific immunoglobulins (especially the 7S) in rabbits with experimental atherosclerosis. Thus, the action of the preparation is realized not by way of direct inhibition of functional activity of the lymphoid tissue cells, but by inhibiting the immunostimulating factor circulating in the blood in experimental atherosclerosis.
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PMID:[The effect of the polyvalent proteinase inhibitor, trasylol, on antibody formation under normal conditions and in experimental atherosclerosis]. 108 67

Lipoprotein(a) is an independent risk factor for cardiovascular disease. Lipoprotein(a) levels were measured in 196 patients (103 Male [M]: 93 Female [F]) with chronic renal diseases and in 116 controls. Median levels of Lipoprotein(a) [Lp(a)] were found to be significantly elevated in patients with untreated chronic renal disease (285,285 mg/L; M,F; range 30-1675 mg/L) and in those treated with continuous ambulatory peritoneal dialysis (320, 603; M,F; range 50-1450) compared with controls (70,51; M,F; range 1-750; p less than 0.01 Males, p less than 0.001 Females). Lp(a) levels in patients treated by haemodialysis (133,35; M,F; range 5-685) and renal transplantation (100,95; M,F; range 10-1700) were not significantly different from controls. Lipoprotein(a) levels correlated inversely with serum albumin in the combined dialysis group (r = -0.34, p less than 0.001), and with urinary protein loss in the combined transplant and chronic renal diseases groups (r = 0.29, p less than 0.01). This correlation of Lp(a) with protein metabolism suggests a similarity with changes in other apolipoprotein-B containing lipoproteins in nephrosis. These findings may be relevant to the increased risk of atherosclerosis in patients with chronic renal disease and to their optimum mode of renal replacement therapy.
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PMID:Lipoprotein(a) levels in chronic renal disease states, dialysis and transplantation. 138 27

Cells of gut, skin, and muscle frequently suffer transient survivable plasma membrane disruptions ("wounds") under physiological conditions, but it is not known whether endothelial cells of the aorta, which are constantly exposed to hemodynamically generated mechanical forces, similarly are injured in vivo. We have used serum albumin as a molecular probe for identifying endothelial cells of the rat aorta that incurred and survived transient plasma membrane wounds in vivo. Such wounded endothelial cells were in fact observed in the aortas of all rats examined. However, the percentage of wounded cells in the total aortic endothelial population varied remarkably between individuals ranging from 1.4% to 17.9% with a mean of 6.5% (+/- 4.6% SD). Wounded endothelial cells were heterogeneously distributed, being found in distinct clusters often in the shape of streaks aligned with the long axis of the vessel, or in the shape of partial or complete rims surrounding bifurcation openings, such as the ostia of the intercostal arteries. Physical exercise (running) did not increase the frequency of aortic endothelial cell membrane wounding, nor did spontaneous hypertension. Surprisingly, 80% of mitotic endothelial cell figures were identified as wounded. This article identified a previously unrecognized form of endothelial cell injury, survivable disruptions of the plasma membrane, and shows that injury to the endothelial cells of the normal aorta is far more commonplace than previously suspected. Plasma membrane wounding of endothelial cells could be linked to the initiation of atherosclerosis.
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PMID:Transient disruptions of aortic endothelial cell plasma membranes. 146 99

Native bovine serum albumin (BSA) was endocytosed and degraded at a steady rate by resident peritoneal murine macrophages with barely detectable amounts remaining within the cells. Radical-damaged BSA was endocytosed and degraded up to 2.5-fold more rapidly than native BSA, but some radical-damaged BSA accumulated within the cells in a time-dependent manner. The extent of accumulation increased in parallel with that of radical damage. Thus, some radical-damaged BSA was processed less efficiently than native BSA. Such inefficient catabolism of radical-damaged proteins may contribute to certain diseases such as atherosclerosis.
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PMID:Accelerated endocytosis and incomplete catabolism of radical-damaged protein. 155 44

We evaluated the safety and efficacy of dextran sulfate low-density lipoprotein (LDL) apheresis in the treatment of three children (aged 6, 7, and 10 years) with severe familial homozygous hypercholesterolemia and undetectable LDL receptor activity. A total of 35 double plasma volume procedures were performed. The ranges of the mean decreases of the three patients in plasma lipid concentrations after LDL apheresis (p less than 0.0001) were as follows: total cholesterol, 76% to 79%; LDL-cholesterol, 78% to 81%; very low density lipoprotein cholesterol, 69% to 75%; high-density lipoprotein cholesterol, 27% to 40%; and triglycerides, 34% to 68%. There were statistically significant but clinically and biologically irrelevant changes in hematologic indexes, serum chemistry values, immunoglobulin levels, complement activity, and plasma concentrations of fat-soluble vitamins. Simple correlation analysis of the variables affecting total cholesterol removal showed significant correlation coefficients (r values) for preapheresis total cholesterol values (r = 0.70; p less than 0.01) and preapheresis LDL-cholesterol values (r = 0.61; p less than 0.01). A multiple regression model explained 82% of the variance based on the preapheresis cholesterol concentration, volume of whole blood processed, and the serum albumin concentration. Side effects of the LDL-apheresis treatments were rare and included abdominal cramping and urticaria. Two procedures were aborted because of intravenous access problems in the younger children. This study confirms that LDL apheresis using a dextran sulfate affinity column is efficacious in rapidly lowering total and LDL-cholesterol concentrations. Furthermore, the procedure is safe and well tolerated by children as young as 6 years of age. This treatment may prevent the progression of atherosclerosis in children with homozygous familial hypercholesterolemia and may therefore avert early death.
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PMID:Treatment of children with homozygous familial hypercholesterolemia: safety and efficacy of low-density lipoprotein apheresis. 159 49

Mouse peritoneal macrophages readily oxidize cholesteryl linoleate/bovine serum albumin emulsions to produce soluble lipid oxidation products, some of the latter being thought to cause cell damage. Mouse peritoneal macrophages were therefore incubated in the presence of cholesteryl linoleate/bovine serum albumin emulsion with and without the addition of dl-alpha tocopherol. The macrophages were observed morphologically and cell damage was estimated by three methods: trypan blue exclusion, lactate dehydrogenase release and tritiated adenine release. All the methods showed significant cell damage which was reduced in the presence of physiological levels of dl-alpha tocopherol. Cholesteryl oleate/bovine serum albumin, which is taken up by macrophages but is not oxidized, was not toxic. dl-Alpha tocopherol was itself toxic in higher concentrations. This self-inflicted macrophage damage might explain the onset of necrosis in atherosclerotic plaques.
Atherosclerosis 1992 Feb
PMID:Cellular damage in mouse peritoneal macrophages exposed to cholesteryl linoleate. 163 53

The relation between serum albumin levels and subsequent incidence of myocardial infarction and coronary heart disease deaths was evaluated using stored serum from the Multiple Risk Factor Intervention Trial (MRFIT). There were 91 coronary heart disease deaths, 113 myocardial infarction patients, and 405 controls matched to cases within 5 years of age, treatment group, and clinic site. There was a highly significant inverse relation between serum albumin level and risk of coronary heart disease. Individuals with a baseline level of serum albumin greater than or equal to 4.7 g/dl had an odds ratio of 0.45 as compared with individuals with a baseline level of serum albumin less than 4.4 g/dl. The relation persisted after adjusting for other cardiovascular risk factors (blood pressure, smoking, and serum cholesterol). The association was stronger for coronary heart disease deaths than for surviving myocardial infarction patients, and for cigarette smokers as compared with cigarette nonsmokers. The deaths studied occurred in the time period at least 6 years after the sera had been obtained and up to 10.5 years of follow-up, and the myocardial infarctions studied occurred within the first 6.5 years of follow-up. There was no consistent relation between time and death due to coronary heart disease or myocardial infarction and albumin levels. Albumin levels are related to the acute phase reaction. Lower albumin levels may be a marker of persistent injury to arteries and progression of atherosclerosis and thrombosis. The consistent relation between albumin and coronary heart disease risk requires further evaluation.
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PMID:The relation between serum albumin levels and risk of coronary heart disease in the Multiple Risk Factor Intervention Trial. 175 41

Dietary fat intake is often regarded as a major determinant of coronary heart disease (CHD) rate and it has been deemed unnecessary to invoke racial or other factors to explain the differences in CHD rates among different ethnic groups. Despite a high prevalence of CHD risk factors such as hypertension, obesity, and smoking, CHD remains a rarity in westernized black Africans. Cord blood total cholesterol (TC), low density lipoprotein cholesterol (LDLC) and apolipoprotein B (apo B) levels were measured and found to be respectively 12.1%, 18.3% and 22.4% lower in black neonates when compared to white neonates. These differences were again studied in a group of young black African males and a comparable group of age-matched whites who had been exposed to the same environment and western diet for at least 2 years. Although the body mass indices and serum albumin concentrations in the adult males were not significantly different, serum levels of TC, LDLC and apo B were 10.7%, 18.7% and 39.7% lower in the blacks, respectively. Furthermore, high density lipoprotein cholesterol (HDLC) and Apolipoprotein AI were 20.2% and 9.5% higher, homocysteine 45.6% lower and coagulation factor VII 26.6% lower in the adult black Africans. It is concluded that blacks are biochemically less responsive to an atherogenic diet than whites and these differences are already present at birth.
Atherosclerosis 1991 Aug
PMID:Ethnic immunity to coronary heart disease? 179 43


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