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

Numerous studies have shown that a limitation of dietary saturated fatty acids and cholesterol associated with an increase in linoleic acid consumption lowers high blood cholesterol level (a risk factor in the development of atherosclerosis). Besides the importance of dietary fatty acid composition in determining blood lipoprotein concentrations, it has been shown that increased intake of dietary linoleic acid influences arterial thrombosis tendency in rats and improves blood platelet function in man. Linoleic acid rich diets also loffer arterial blood pressure in salt loaded rats and in hypertensive men. Moreover, these diets improve heart function in rats as measured by coronary perfusion rate and ventricular work. These favourable effects of linoleic acid on various risk factors of cardiovascular diseases are observed at dietary levels which largely exceed the minimum amount required to prevent or cure the essential fatty acid deficiency syndrome. It is evident that the study of the physiological effects of linoleic acid goes beyond the scope of this syndrome. Essential fatty acids have structural functions as integral part of membrane phospholipids and dynamic functions as precursors of prostaglandins. On account of their structural function, the essential fatty acids influence the fluidity of biomembranes and the activity of membrane-bound enzymes and receptor systems. Certain physiological effects of dietary linoleic acid would be explained via this mechanism. Moreover linoleic acid is known to regulate the endogenous prostaglandin biosynthesis. Though incomplete, the knowledge gained fully justifies the application of preventive measures proposed by numerous expert committees for groups of populations with a high rate of atherosclerosis.
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PMID:[Essential fatty acids in cardiovascular physiopathology]. 700 87

This study describes a variant of hypo-alpha-lipoproteinemia in a 57-year-old male patient. The total plasma cholesterol level was 258 mg/dl with 64% in esterified form. The concentration of triglycerides was 205 mg/dl. The lipoprotein electrophoretic pattern revealed the absence of alpha-lipoproteins, whereas the other lipoproteins showed an intermediate electrophoretic mobility. The concentration of HDL cholesterol (heparin: MgCl2 precipitation) was extremely low (3 mg/dl). The activity of lecithin; cholesterol acyltransferase (LCAT) and the postheparinlipolytic activity were within the normal range. Determination of apolipoproteins revealed a marked deficiency of both apoprotein A-I (17 mg/dl) and apolipoprotein A-II (11 mg/dl). The concentration of apolipoprotein-B was elevated (186 mg/dl). Unlike the clinical manifestations of Tangier disease, our patient did not show skin lesion, abnormal tonsils, hepatosplenomegaly, peripheral neurologic abnormalities or corneal deposits. Also in contrast to Tangier disease our patient had coronary artery disease with myocardial infarction accompanied with severe occlusive peripheral arterial disease.
Atherosclerosis 1982 Mar
PMID:Hypoalpha-hyperbeta-lipoproteinemia in a patient with coronary artery disease and occlusive peripheral arterial disease. 708 13

In electromicroscopic studies of remodelling atherosclerosis in rabbits collagen fibers within smooth muscle cells of atherosclerotic lesions were observed. Their most common appearance was in form of elongated membrane-bound profiles enclosing single banded collagen fibers with a diameter corresponding to that of extracellular collagen. The unit membranes were in apposition to the fibers, that were generally linear or slightly curved. In other instances small groups of collagen fibers lay packed together within larger compartments; still other cytoplasmic vacuoles contained structures hardly recognizable as collagen fibers. In all the cases membranes bordering collagen fibers were free of ribosomes, smooth surfaced. The presence of collagen fibers within smooth muscle cells is regarded as morphological expression of phagocytosis and decomposition of extracellular collagen in remodelling atherosclerotic lesions.
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PMID:Degradation of collagen fibers by intimal smooth muscle cells in remodelling atherosclerotic lesions in rabbits. 721 37

When experimental animals are kept on an atherogenic diet the NADP.H-dependent phospholipid deoxygenase in the membranes of the hepatic endoplasmic reticulum is activated and the degree of membrane oxidation is increased. "Peroxide" modification of microsomal membranes is attended by changes in their conformation and as a consequence, changes in the activity of membrane-bound enzymes. Proceeding from the fact that the synthesis of the components and the assembly of the supramolecular lipoprotein structure as well as cholesterol catabolism are accomplished by the enzyme systems localized in the hepatic microsomes, the role of peroxidation of the microsomal lipids in the pathogenesis of atherosclerosis is discussed.
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PMID:[Lipid peroxides and atherosclerosis. Hypothesis: the role of cholesterol and free-radical lipid peroxidation in altering cell membrane properties in hypercholesterolemia and atherosclerosis]. 741 95

Vascular remodeling is a key process in the pathophysiology of atherosclerosis. Recent evidence suggests that high glucose levels may function as a vascular smooth muscle growth and proliferation-promoting substance. To explore the role of the polyol pathway in this process, we examined the effect of an aldose reductase inhibitor (ARI), epalrestat, on the growth characteristics of cultured rat vascular smooth muscle cells (VSMCs). Epalrestat (10 nmol/L, 1 mumol/L) significantly suppressed the high glucose-induced proliferative effect as measured by [3H]thymidine incorporation by 67% and 82% in cell number, suggesting ARI as an antimitogenic factor. In VSMCs, epalrestat (10 nmol/L, 1 mumol/L) significantly suppressed the high glucose-induced incorporation of [3H]leucine by 45% and 58% with the concomitant reduction of the cell size estimated by flowcytometry. Epalrestat (1 mumol/L) also suppressed high glucose-induced intracellular NADH/NAD+ increase and membrane-bound protein kinase C activation. These results indicate that this ARI possesses an antiproliferative and antihypertrophic action on VSMCs induced by high glucose possibly through protein kinase C suppression.
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PMID:Aldose reductase inhibitor prevents hyperproliferation and hypertrophy of cultured rat vascular smooth muscle cells induced by high glucose. 748 44

Endothelium-derived relaxing factor/nitric oxide (EDRF/NO) is produced by the vascular wall and is a key modulator of vascular tone and blood pressure. Since reduced EDRF/NO release from the endothelium is a major key event in the development of atherosclerosis, we investigated the effect of cholesterol on endothelial cell particulate (membrane-bound) NO synthase activity. Low concentrations (up to 0.2 mM) of liposomal cholesterol progressively activated plasma membrane-bound NO synthase. Increasing cholesterol concentration above that which maximally stimulated enzyme activity produced a progressive inhibition with respect to the control value. In time course experiments using endothelial cell plasma membranes enriched with cholesterol, changes in NO production were followed by analogous changes in soluble guanylate cyclase activity (sGC). N-Monomethyl-L-arginine (L-NMMA) (1 mM) inhibited particulate NO synthase activity at all cholesterol concentrations used with subsequent decreases in cGMP production. Egg lecithin liposomes (free of cholesterol) had no effect on NO synthase activity. A three-fold increase in superoxide (O2-) and a 2.5-fold increase in NO formation followed by an eight-fold increase in peroxynitrite (ONOO-) production by cholesterol-treated microsomes isolated from endothelial cells was observed, one which rose further up to eight-fold in the presence of superoxide dismutase (SOD) (10 U/mL). Cholesterol had no effect on Lubrol-PX solubilized membrane-bound NO synthase or on cytosolic (soluble) NO synthase activities of endothelial cells. Cholesterol modulated lipid fluidity of plasma membranes labelled with 1,6-diphenyl-1,3,5-hexatriene (DPH) as indicated by the steady state fluorescence anisotropy [(ro/r)-1]-1. Arrhenius plots of [(ro/r)-1]-1 indicated that the lipid phase separation of the membranes at 26.2 +/- 1.5 degrees was elevated to 34.4 +/- 1.9 degrees in cholesterol-enriched membranes, consistent with a general decrease in membrane fluidity. Cholesterol-enriched plasma membranes treated with egg lecithin liposomes showed a lipid phase separation at 27.5 +/- 1.6 degrees, indicating the reversible effect of cholesterol on membrane lipid fluidity. Arrhenius plots of NO synthase activity exhibited break point at 26.9 +/- 1.8 degrees which rose to 35.6 +/- 2.1 degrees in 0.5 mM cholesterol-treated plasma membranes and decreased to 21.5 +/- 1.4 degrees in plasma membranes treated with 0.2 mM cholesterol. The allosteric properties of plasma membrane-bound NO synthase inhibited by Mn2+ (as reflected by changes in the Hill coefficient) were changed by cholesterol, consistent with modulations of the fluidity of the lipid microenvironment of the enzyme.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Modulation of particulate nitric oxide synthase activity and peroxynitrite synthesis in cholesterol enriched endothelial cell membranes. 754 Mar 91

The aim of this study is to evaluate the correlation between a rise in blood neutrophil concentration and cellular and molecular changes of erythrocytes, among populations presenting an increased risk of cardiovascular disease (CVD). A population of men aged 20-65 years was used which included 22 post-myocardial infarction individuals (< 48 h), 24 survivors of myocardial infarction (> 3 months), 12 hypertensive individuals and 29 individuals presenting normal haematological values and normal lipid profile. The lipid profile parameters used to ascertain increased risk of CVD included triglycerides (TG), total cholesterol (Chol), high-density lipoprotein cholesterol (HDLc), low-density lipoproteins cholesterol (LDLc) and apolipoproteins A1 (Apo A1) and B (Apo B). The hematological parameters measured were concentration of total white blood cells (WBC) and of the several leukocyte types; concentration of red blood cells (RBC); hematocrit (Ht); hemoglobin concentration (Hb); mean cell volume (MCV); activity of erythrocyte glucose-6-phosphate dehydrogenase (G6PD); band 3, its aggregates and fragments in erythrocyte membranes, the percentage of membrane-bound hemoglobin (MBH), and the linkage of immunoglobulin G (IgG) to erythrocyte membrane. We found that the MBH and the band 3 profile is different in control as compared to pathological groups and that, as expected, the aggregation of band 3 promotes the linkage of IgG to the erythrocyte membrane. A negative correlation was shown between total neutrophils and both total RBCs and erythrocyte G6PD activity. We suggest that the erythrocyte, a cell that undergoes and accumulates oxidative and proteolytic damage along its life span, may provide a useful model of oxidative and proteolytic stress in CVD and that band 3 may represent a useful marker of that stress.
Atherosclerosis 1995 Aug
PMID:Altered erythrocyte membrane band 3 profile as a marker in patients at risk for cardiovascular disease. 757 75

Evidence is accumulating that most of the degenerative diseases that afflict humanity have their origin in deleterious free radical reactions. These diseases include atherosclerosis, cancer, inflammatory joint disease, asthma, diabetes, senile dementia and degenerative eye disease. The process of biological ageing might also have a free radical basis. Most free radical damage to cells involves oxygen free radicals or, more generally, activated oxygen species (AOS) which include non-radical species such as singlet oxygen and hydrogen peroxide as well as free radicals. The AOS can damage genetic material, cause lipid peroxidation in cell membranes, and inactivate membrane-bound enzymes. Humans are well endowed with antioxidant defences against AOS; these antioxidants, or free radical scavengers, include ascorbic acid (vitamin C), alpha-tocopherol (vitamin E), beta-carotene, coenzyme Q10, enzymes such as catalase and superoxide dismutase, and trace elements including selenium and zinc. The eye is an organ with intense AOS activity, and it requires high levels of antioxidants to protect its unsaturated fatty acids. The human species is not genetically adapted to survive past middle age, and it appears that antioxidant supplementation of our diet is needed to ensure a more healthy elderly population.
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PMID:The role of free radicals in disease. 761 52

Matrix production by smooth muscle cells (SMC) appears to play a major role in the intimal thickening process. Proteoglycans (PG) are the predominant extracellular matrix component of early restenotic lesions. As angiotensin II (A II) has been proposed as a mediator of restenotic process, we hypothesized that A II may directly affect PG synthesis by SMC. SMC were cultured in the presence of [35S]sulfate and angiotensin II, and both the secreted and membrane-bound proteoglycans were analyzed. A II (1 to 100 nM) evoked a dose- and time-dependent increase in both cell- and media-associated PG production, an effect abrogated by the A II receptor antagonist, saralasin. SMC constitutively synthesize small amounts of PG with a molecular mass of 170-250 kDa. After treatment with A II, the abundance of PG is increased, as well as its molecular mass (230-300 kDa). Selective degradation by chondroitinases and heparinase identified chondroitin and dermatan sulfate PG as the predominant form being induced. These results demonstrate that the effect of A II is not general and is specific to certain classes of PGs. In order to further examine the specificity of the A II effect, we compared the synthesis of PG induced by A II with that induced by platelet-derived growth factors AA and BB (PDGF-AA and -BB), insulin-like growth factor I (IGF-I), and tumor necrosis factor alpha (TNF alpha). This comparison demonstrated that the profile of PG induced by A II is different from the other factors examined. Taken together, these data indicate that A II may not only function as a hypertrophic factor for SMC, but in addition may also be a potent modulator of specific PG synthesis by these same cells, which could significantly contribute to the formation of atherosclerotic and restenotic lesions.
Atherosclerosis 1994 Nov
PMID:Stimulation of rat vascular smooth muscle cell glycosaminoglycan production by angiotensin II. 784 Aug 14

We describe the cardiovascular state of a 60-year-old homozygous patient with familial HDL deficiency (Tangier disease). The patient was examined by coronary angiography and intravascular ultrasound because of chest pain at rest and on exertion. We found a normal left ventricular function, moderately diffuse coronary sclerosis without stenosis and no critical stenosis of peripheral arteries. Intravascular ultrasound revealed the three layer appearance of arterial intima, media and adventitia with normal thickness. No calcified plaques or intimal hyperplasia could be detected apart from a single, discrete atherosclerotic lesion in one iliac artery segment. Concentric non-occlusive atherosclerotic lesions which are readily detectable with intravascular ultrasound were not found. The lack of severe atherosclerosis was remarkable insofar as massive foam cell formation and the virtually complete absence of circulating HDL is characteristic of Tangier disease and has been previously demonstrated in this patient. Our findings suggest that HDL deficiency and foam cell formation in Tangier disease are not necessarily associated with accelerated development of atherosclerosis.
Atherosclerosis 1994 Oct
PMID:Characterization of atherosclerosis in a patient with familial high-density lipoprotein deficiency. 784 70


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