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)

A number of soluble proteins contained in human aortic intimal tissue was extracted into buffered saline (pH 7.4) and identified and quantitated by immunoelectrophoresis and immunodiffusion. The proteins included IgA, IgG, IgM, B1C (C3), alpha 1-antitrypsin, alpha 2-macroglobulin, fibrinogen, albumin, LDL, HDL, alpha 1-acid glycoprotein, beta 2-glycoprotein, transferrin and ceruloplasmin. The concentration of soluble proteins was significantly higher in the atherosclerotic intima than in the normal intima. The diseased intima also contained a small amount of tissue-bound IgG, IgA and B1C which was extractable with citrate buffer at pH 3.2. The vascular band IgG, and B1C were shown by enzymatic and immunohistochemical studies to be closely associated with the collagenous tissue of the plaque. The Ig contained in the atherosclerotic plaque may be derived in part from the biosynthesis of Ig by the artery, since the incorporation of 14C-labeled leucine into IgG by the atheromatous plaque was demonstrable by radioimmunoelectrophoresis. In contrast to the diseased artery, the normal artery did not synthesize IgG and did not contain vascular bound IgG or complement. However, the normal artery was capable of fixing IgG and B1C eluted from the diseased artery. The present studies suggested that the IgG contained and synthesized by the plaque might represent an immune response to an endogenous or exogenous antigen closely associated with plaque collagen. IgG and B1C either alone or in the form of an immune complex also may play an important role in phagocytosis in the plaque and thereby influence the course of atherosclerosis. The proteolytic inhibitors, alpha 1-antitrypsin and alpha 2-macroglobulin, found in relatively high concentrations in the plaque, could enhance fibrosis of the lesion because of thier known inhibitory effects on collagenase and elastase.
Atherosclerosis 1979 Dec
PMID:Soluble proteins in the human atherosclerotic plaque. With spectral reference to immunoglobulins, C3-complement component, alpha 1-antitrypsin and alpha 2-macroglobulin. 9 93

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

The effect of nicotinic acid was investigated in Rhesus monkeys. Subcutaneous injections of nicotinic acid lower the plasma very low density lipoprotein (VVLDL) and low density lipoprotein (HDL) concentration. The fall in LDL concentration is not accompained by any change in the lipid or protein composition of either lipoprotein. Analysis by Sephadex gel chromatography and polyacrylamide-gel electrophoresis showed that the proteins of monkey VLDL and LDL are qualitatively similar to those of human VLDL and LDL, although there are differences in the proportions of the various proteins present in the two species. Subcutaneous injections of nicotinic acid diminish the maximum incorporation of 14C from [14C]threonine into VLDL and LDL apoproteins, but have no effect on incorporation into albumin or HDL apoprotein. Peak incorporations into the apo-B and apo-C of VLDL are diminished to about equal extents by nicotinic acid. Comparison of the amount of 14C lost from apo-B of VLDL after the peak of incorporation, with that gained by apo-B of LDL during the same period, suggests that some of the circulating apo-B of LDL IS DERIVED FROM SOURCES OTHER THAN CIRCULATING VLDL.
Atherosclerosis
PMID:The effect of nicotinic acid on the metabolism of the plasma lipoproteins of rhesus monkeys. 16 24

Two classes of pig plasma low density lipoprotein (LDL1 and LDL2) with different densities and molecular sizes were isolated by zonal ultracentrifugation and were further purified by flotation. The peptide component was iodinated with 125I, and the labelled lipoprotein was injected intravenously. 125I-LDL1 turnover studies were performed on 22 3-4 month old female Large White pigs, and 125I-LDL2 turnover studies on 4 similar pigs. A biological screening experiment confirmed that the shape of the plasma activity curve was not a function of protein denaturation. The pattern of radioactivity decline in plasma was not affected by the degree of LDL iodination. 125I-LDL1 turnover: The curve of plasma radioactivity plotted against time over the first 5 days after injection could be resolved into two exponentials. The plasma biological half-life (T 1/2) was calculated from the slower exponential predominant from the second day. The mean T 1/2 over 2-5 days was 22.9 hr (range 17.2-28.5 hr). Multicompartmental analysis of the plasma decay curve using an open mammillary model gave a mean fractional catabolic rate per day for LDL1 of 1.4 (range 0.9-1.9). The mean T 1/2 was 0.26-0.31 times and the fractional catabolic rate 3.0-3.9 times those values found in two studies on adult humans. The tissue distribution of 125I was analysed in a series of 20 animals killed from 1.0 to 33.8 days after 125I-LDL1 injection. Most tissue 125I (86-89%) was protein bound. An appropriate correction was made to the 125I counts for retained plasma in liver and spleen (using 131I-albumin); retained plasma in other tissues was negligible. Highest 125I tissue levels were found in the liver, supporting other evidence that the liver may be the major site of LDL1 catabolism. After 2.06 and 4.06 days the livers in two animals contained 1.6% and 0.7% respectively of the total injected 125I, equal to 33% and 54% of the total plasma 125I at those times. The skin contained about one-third to one-ninth the 125I in the liver at various times. Distribution in other organs was quantitatively minimal. Higher levels of radioactivity were found in the intima and inner media of the aorta than in the outer media. These results suggest that plasma LDL in the pig diffuses through the endothelial surface into the arterial wall. These findings are confirmed by autoradiography. 125I-LDL2 turnover: Parallel studies of plasma 125I-LDL2 turnover and tissue distribution were performed. The plasma biological decay curve was multi-exponential, suggesting that LDL2 metabolism is complex, and possibly more rapid than that of LDL1 (LDL2 is smaller and denser than LDL1). The tissue distribution of 125I-LDL2 in these pigs was very similar to that of 125I-LDL1. As LDL1 and LDL2 differ in the amount of lipid they contain, they may have different roles to play in lipid transport, and there may be interconversion of one into the other at different sites. This hypothesis remains conjectural.
Atherosclerosis
PMID:The plasma and tissue turnover and distribution of two radio-iodine-labelled pig plasma low density lipoproteins. 17 56

Effects of partial inhibition of aortic histamine formation on aortic albumin uptake and lipid deposition were examined in male, New Zealand white rabbits maintained on Purina Rabbit Chow containing 0.5% cholesterol for a 2-week period. Aortic histamine synthesis was inhibited by partial inhibition of aortic histidine decarboxylase (HD) through administration of alpha-hydrazinohistidine (alpha-HH, MK785, Regis Chemical Co., 25 mg/kg, i.p. at 12-h intervals). Additional rabbits were maintained on either the cholesterol diet or on Purina Rabbit Chow without cholesterol. Results indicate that administration of alpha-HH for the 2-week period produced a 31% reduction (P less than 0.05) in aortic HD activity in those rabbits maintained on the cholesterol diet, and that concurrently there was a 51% reduction in aorta albumin uptake (P less than 0.025) and a 63% reduction in the extent of oil red O staining. By regression analysis a significant correlation coefficient (r = 0.71, P less than 0.005) was obtained between the aortic albumin uptake and the aortic histamine forming capacity (HFC) in rabbits maintained on this cholesterol diet. These findings indicate that the aortic HD system may be an important enzymatic coupler involved in vascular permeability alterations occurring early in the atherogenic sequence.
Atherosclerosis 1979 Dec
PMID:Relationship between inhibition of aortic histamine formation, aortic albumin permeability and atherosclerosis. 51 43

Fasting plasma concentrations of triglycerides (TG), cholesterol, immunoreactive insulin (IRI), and blood glucose were raised in 16 children with chronic renal failure on regular haemodialysis compared with 18 healthy children. In the patients plasma IRI correlated positively with plasma TG, while blood glucose did not correlate with IRI or lipid concentrations. Dietary intake, expressed as percentage of recommended intake for height-age, did not correlate with plasma lipids, but there was a positive correlation between plasma TG and the proportion of calories derived from carbohydrate. The children were not malnourished as evidenced by normal plasma albumin and transferrin concentrations. The mechanism of the hyperlipidaemia is unclear but it may be related to the glucose intolerance with hyperinsulinaemia which is found in uraemia. In view of the risk of premature atherosclerosis, plasma lipid concentrations should be monitored in children with chronic renal failure and attempts made to ameliorate hyperlipidaemia with appropriate dietary manipulations.
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PMID:Hyperlipidaemia in children on regular haemodialysis. 60 69

Because atherosclerosis may be reversible, a routine noninvasive screening test for the reliable diagnosis of mild coronary arterial lesions would allow potential prevention of coronary events in specific patients through intensive dietary management, drug therapy and physical training. To determine the minimal coronary stenosis detectable with myocardial perfusion imaging techniques, standardized stenoses ranging from 31.4 to 72.5 percent diameter narrowing were applied to the left circumflex coronary artery of 12 open chest dogs. Indium-113m-labeled human albumin microspheres were injected into the left atrium under control conditions and technetium-99m human albumin microspheres during maximal coronary vasodilatation induced with intravenous dipyridamole. Hearts were removed, sliced into 1 cm thick cross sections and imaged under a gamma camera. The results demonstrate that 40 percent diameter coronary stenoses can be identified by imaging relative subendocardial underperfusion during pharmacologic coronary vasodilatation. An imaging technique sensitive enough to identify mild coronary lesions for diagnostic screening purposes requires (1) a potent stimulus for coronary vasodilatation, such as intravenous dipyridamole; (2) an imaging agent taken up by the myocardium in proportion to coronary flow at flow rates up to four or more times resting coronary flow so that differences in regional maximal flows caused by mild stenoses can be identified; and (3) cross-sectional tomographic myocardial imaging to visualize relative endocardial-epicardial perfusion, the most sensitive indicator of the hemodynamic effects of coronary stenoses, and to exclude from the imaging field the interfering activity of lung, background and overlying heart structures.
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PMID:Assessment of coronary stenoses with myocardial perfusion imaging during pharmacologic coronary vasodilatation. IV. Limits of detection of stenosis with idealized experimental cross-sectional myocardial imaging. 70 89

Hyperlipemic stilboestrol-treated cockerels, cholesterol-fed rabbits and minipigs, as well as normolipemic cockerels and rabbits were injected intravenously with homologous plasma of corresponding lipid concentration labelled in vivo with radioactive cholesterol. The ratios between labelled free cholesterol and labelled esterified cholesterol in the intima--media from the thoracic aorta of these 5 groups of animals were respectively 1-, 2-, 8-, 2- and 20-fold greater than the corresponding average tracer ratio in plasma during the uptake period of 4--6 h. The intima--media tissue in the coronary arteries studied in one minipig contained 2--5 times more labelled cholesterol per mg wet weight than corresponding aortic tissue. This arterial uptake of labelled cholesterol in the minipigs was measured concomitantly with the uptake of phosphatidylcholine and plasma protein labelled in vivo. The uptake for these various tracers in the minipig suggested entry of labelled free and esterified cholesterol into the arterial wall, mainly as part of the plasma lipoproteins, with subsequent hydrolysis in the arterial wall of some of the cholesterol ester. In the stilboestrol-treated cockerels hydrolysis of cholesterol ester seems to be absent. The relatively higher uptake in the minipig of the labelled plasma protein (albumin) than of the lipoprotein (as traced by its lipids) suggests a molecular weight-dependent arterial entry of these plasma macromolecules.
Atherosclerosis 1978 Nov
PMID:Uptake of labelled free and esterified cholesterol from plasma by the aortic intima--media tissue measured in vivo in three animal species. 71 37

Two new permeability tests are described for use with intravenously injected trypan blue. One depends on the demonstration of trypan blue by its specific red fluorescence in green light at 570 nm, while the other is a surface microscopy technique at low magnification, using illumination from a fibre-optics light source. The routes of entry of the trypan blue-albumin complex into the rat and rabbit aorta appear to be from both the inner and outer surfaces. Over the period 1/4-24 h after injection of the dye, more entered from the outer surface than the inner surface in the rat aorta and rather more in the rabbit thoracic aorta. The arch of the rabbit aorta showed in general rather greater entry from the inner surface. Trypan blue that has entered the aortic wall is partly taken up by the elastic lamellae. Elastic competes successfully for the dye and captures it from the trypan blue-albumin complex; this uptake is blocked by deamination with nitrous acid.
Atherosclerosis 1977 Apr
PMID:Permeability of inner and outer layers of rat and rabbit aortic wall. Two new microscopic test with trypan blue. 85 6

A new microscopic fluorescence method for trypan blue at 570 nm has been used to follow the entry of albumin into the atheromatous rabbit aorta. Permeability into the inner aortic wall increases before the onset of gross lesions and seems just to precede intraendothelial deposition of lipid. Thereafter, permeability of the inner wall progressively increases until streaks or small plaques develop. These raised lesions stain and fluoresce variably, some intensely so while others are almost unreactive. This variability might reflect the difference between progressive and quiescent lesions. However, a zone of increased permeability surrounds many raised lesions, suggesting that the edge is a major site of growth and progression.
Atherosclerosis 1977 Jul
PMID:Permeability in atherosclerosis: fluorescence test in green light with trypan blue. 90 31


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