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

Cholesterol binds to streptolysin O and related bacterial toxins. In normal serum, only a fraction of the cholesterol attached to lipoprotein is available for binding, probably as a cholesterol-peptide complex formed during catabolic breakdown of the lipoprotein. Cholesterol esterase produced by certain organisms--e.g., Staphylococcus pyogenes and Pseudomonas oeruginosa--augments this fraction both in vitro and in vivo. Endogenous esterase similarly increases the amount of cholesterol-peptide complex, a mechanism which may be activated as a feedback process following binding of toxin to the cholesterol component of the complex. These complexes will thus supply a readily available means of binding bacterial toxins before antibody formation begins; Cholesterol-peptide complexes, either alone or modified by binding to toxin, may function as autoantigens. It is postulated that immune complexes so formed may be involved in atherosclerosis either by directly damaging vessels walls or by cross-reaction of antibody with cell-membrane-bound lipoproteins which equilibrate with plasma-lipoproteins.
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PMID:Functional role of cholesterol in infection and autoimmunity. 4 49

The first stages of the atherosclerotic lesions induced in the rabbit aorta by adrenalin- thyroxine, with (or without) an hypercholesterolic diet, have been studied on the 6th, 13th, and 22nd day. Major parietal changes, barely demonstrable with light microscopic standard techniques, were detected, as soon as the 6th day, by electronmicroscopy and histoenzymology. These changes were probably due solely to the hormonal treatment. In the early stage, they consisted of some fragmentations of the elastic sheets and some smooth muscle cell lysis. The oxidative and ATPase activities were greatly reduced. The increased lysosomal hydrolase actitivities of the outer layers of the vessel could be related in the increased vascular permeability and consecutive increased perfusion gradient induced by these lesions. Later, an obvious repair process was seen. The smooth muscle cells bearing numerous processes were bound by many microfilaments and by some elastic material. The energetic enzymatic activities were increased. The part taken by the lipidic diet in these changes, apart from the increase of the esterase activity, did not seem yet of significance in this first stage of atherosclerosis. However, one cannot exclude that the intensively accumulating lipids might, at some later stages, potentiate the consequences of the vascular lesions or impede the repair process.
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PMID:[Early histoenzymologic and ultrastructural changes induced by adrenalin-thyroxine and fat diet in rabbit aorta (author's transl)]. 17 72

Six strains of genetically defined JAX rabbits were tested for their serum cholesterol levels (total and free) in response to a 0.5% cholesterol diet. Marked differences in response between the 6 strains were found. IIIVO/J and WH/J are low responding strains, X/J and ACEP/J are intermediate responding strains, and OS/J and AX/J are high responding strains. After 4 weeks of the cholesterol diet the total serum cholesterol level of the high responding AX/J strain was about 5-fold greater than the level of the low responding IIIVO/J strain. The esterified/total (E/T) ratio appeared to be higher in the high responding strains, indicating a synergistic effect in the process of atherosclerosis. The response of the individual rabbits to the cholesterol diet was compared with the patterns of serum and liver esterase zymograms. This comparison indicated a correlation of the dietary cholesterol susceptibility with the presence or absence of the esterase zones in the anodal, fast moving region of the gel.
Atherosclerosis 1977 Dec
PMID:Strain differences in response to dietary cholesterol by JAX rabbits: correlation with esterase patterns. 59 51

The effect of hypertension, which is known to enhance atherosclerosis, on acid esterase activity of rat aortic wall was studied histochemically. The purpose was to test our notion that atherogenesis depends on the balance between supply of lipids to the arterial smooth muscle cells and the lysosomal esterase activities. Hypertension was produced in rats by unilateral nephrectomy and administration of desoxycorticosterone acetate and sodium chloride. The animals reacted with varying degrees of hypertension. In rats with hypertension of a sufficiently high degree and of long duration, inhibition of aortic acid esterase activities occurred. No inhibition of these enzymes occurred in the other organs examined.
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PMID:Experimentally produced hypertension and aortic acid esterase. 98 72

Most of the linkage of atherosclerosis and thrombosis with estrogens is epidemiologic in origin. Although the effects of estrogens on the mechanisms of hemostasis are wide ranging, many are benign; only a few may account for thrombus formation. Platelet function tests have provided extensive but contradictory data, and interpretation is limited because it is uncertain whether a rise in one or more of these parameters is a primary or secondary effect. The most consistent effects of estrogens on coagulation proteins are elevations of fibrinogen; factors II, VII, IX, X, and XII; protein C; and plasminogen. Although these elevations have been attributed to the estrogenic component in oral contraceptives, the progestogen concentration may also influence these increases. Among other coagulation proteins studied, the following are unaffected by oral contraceptive use: factors V, VIII, and XI; prekallikrein; and high-molecular-weight kininogen. In contrast, protein S values are decreased. The plasma concentration of plasmin inhibitor is unchanged, whereas both proteinase inhibitor and macroglobulin are significantly increased by oral contraceptive use. Cl esterase inhibitor is decreased in women taking oral contraceptives and correlates with the increase in Hageman factor. Antithrombin III is one plasma inhibitor for which a decrease in quantity and activity have been associated with a thrombotic tendency in humans. Although data on estrogen-associated changes in the quantity of antithrombin III have been conflicting, the ability of plasma to inhibit factor Xa is significantly reduced in a dose-dependent manner among pre- and postmenopausal estrogen users.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Estrogen-associated thromboembolism. 134 94

The main objective of the study was to investigate the effect of the calcium antagonists Verapamil (2 mg.kg-1.day) and Nifedipine (1 mg.kg-1.day-1) on cholesterol (1%) induced atherosclerosis in rabbits. The drugs were administered s.c. twice daily over a period of 8 weeks. Blood lipid levels were determined three times during the experiment. After the experimental period the animals were killed and macroscopic changes on the aorta were recorded. For histochemical investigation samples were taken from the arch of the aorta and coronary artery. In cryostat sections lipids were determined by Sudan black B and Fett rot 7 B and the following enzymes were assayed: acid phosphatase, non-specific and acid esterase, acid beta-galactosidase, dipeptidyl peptidase I and II, and glucose-6-phosphate dehydrogenase. Following treatment with the calcium antagonists the levels of triacylglycerols and of total cholesterol were significantly increased in comparison with the control and diet groups. The ratio of HDL cholesterol to total cholesterol decreased in the treated animals. In lipoid plaques the activity of enzymes was enhanced in all experimental animals. There were however no qualitative differences in the composition of plaques between individual groups, which exhibited only quantitative differences. The number of migrating macrophages was increased only in the nifedipine treated animals. The extent of plaques was significantly decreased after nifedipine treatment, whereas verapamil failed to exert antiatherogenic effect. (Tab. 2, Fig. 4, Ref. 22.).
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PMID:[The effect of verapamil and nifedipine on the development of experimental atherosclerosis in rabbits]. 152 79

Leukocyte adhesion and other injury parameters have been studied in the aortic endothelium of Sprague-Dawley rats in two situations: (1) spontaneous pathology in conventional rats with antibodies to Mycoplasma pulmonis and/or Kilham or Sendai viruses, and (2) intravascular coagulation by thrombin administration in SPF rats. Adhesion (esterase (+) leukocytes/mm2) in SPF rats was 8 +/- 5 (n = 12). Adhesion in 38% of the conventional rats was 54 +/- 27 (n = 8), half of them being non-analyzed and the rest having antibodies to M. pulmonis and/or Kilham rat virus. In 19 rats with antibodies to M. pulmonis and/or Kilham or Sendai viruses, AgNO3 and hematoxylin staining of the aortic endothelium showed an increase in leukocyte adhesion, and the presence of argyrophilic cells, stigmata and granularity--severe endothelial lesions being observed in some cases. Adhesion in rats after 0.25, 1, 3 and 6 h of thrombin administration (30 units/100 g) was not different from controls. Adhesion after 24 h was 108 +/- 53 (n = 10) and 60 +/- 59 (n = 10), and 22 +/- 20 (n = 10) in rats treated with thrombin plus heparin or hirudin, respectively. Thrombin produced endothelial lesions at all times studied, and these included membrane blebs, platelet and erythrocyte adhesion and alterations in the pattern of endothelial esterase activity.
Atherosclerosis 1992 Apr
PMID:Effect of spontaneous pathology and thrombin on leukocyte adhesion to rat aortic endothelium. 159 Aug 26

Scanning electron microscopy, impregnation, histochemical methods with acetylcholine esterase (AChE), choline acetyltransferase and glyoxylic acid were used for studying elements of afferent and efferent (+ adrenergic and cholinergic) innervation of pial arteries 450-60 microns in diameter in persons with "preclinical" atherosclerosis. Marked changes of the nervous system were found in arteries of large calibre. Disorders were seen in afferent innervation with increased crimp in nervous fibers, alternate patches of hypo- and hyperimpregnation, thickening with a high AChE activity, reactive changes in receptors. The structure of choline- and adrenergic nervous plexuses was disordered; the concentration of nervous fibers and varicosities in particular in fluorescent plexuses was decreased, with a moderate increase in the concentration of these structures being seen in cholinergic plexuses.
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PMID:[Innervation of human pia mater arteries of different diameters in arteriosclerosis]. 196 69

Mononuclear phagocytes adhere to and penetrate the vessel wall endothelium and contact the subendothelial space prior to the development of the atherosclerotic plaque. In an attempt to model the early events of plaque development we used an elastin-rich, multicomponent, cell-derived matrix from neonatal rat aortic smooth muscle cells as a substratum for monocytes. Using this model, we show that human monocyte morphology and metabolism are markedly altered by the matrix substratum. When a mixed mononuclear cell population is seeded on matrix or plastic, only monocytes adhere to the matrix surface. In contrast, lymphocytes as well as monocytes adhere to the plastic surface. The matrix-adherent monocytes develop large intracellular granules and form extensive clusters of individual cells. Metabolically, these cells develop sodium fluoride resistant non-specific esterase activity and their media contain more growth factor activity and PGE2. Although total protein synthesis is equivalent in both cultures, the matrix contact induces an increase in specific proteins in the media. We also show that a purified alpha-elastin substratum induces some, but not all, of the monocyte changes seen when using the matrix substratum. Using the alpha-elastin substratum, there is selective adhesion of monocytes and increased growth factor activity, however, the cells are morphologically different from the matrix-adherent cells. Thus, the use of the smooth muscle cell-derived matrix, in conjunction with purified matrix components, serves as a model that can provide insight into the mechanisms of monocyte adhesion and stimulation by the matrix environment that exists in vivo. Such mechanisms may be particularly important in atherogenesis.
Atherosclerosis 1990 Dec
PMID:Monocyte activation by smooth muscle cell-derived matrices. 210 75

Cellular components of the bronchovascular barrier have been studied in human lungs obtained after death of some patients with acute and chronic lung inflammatory diseases, hypertonic disease, atherosclerosis and chronic glomerulonephritis. Certain oxidative-reductive and hydrolytic enzymes, including NAD-, NADP- diaphorases, lactic dehydrogenase, acid and alkaline monophosphoesterase, ATP-ase, adenylate cyclase and nonspecific esterase were evaluated quantitatively after the histochemical processing of the specimens for the above reactions. Correlation analysis was performed for the bronchial epithelium, endotheliocytes, lymphocytes, plasma and mast cells, as well as macrophages and polymorphonuclear leucocytes. The results showed that there was a significant shift in some of the measured enzymic activities. Moreover, the correlations between different quantitative data were noted and these correlations changed with age. The increase in "rigidity" of the correlations in the elements of the bronchovascular barrier has been demonstrated during the process of ageing.
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PMID:Functional morphology of the bronchovascular barrier of the human lungs during various age periods. 214 10


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