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)

2-(2,4-Dimethylphenyl)indan-1,3-dione was shown to be a potent hypolipidemic agent in rodents, lowering significantly both serum cholesterol and triglyceride levels at 20 mg/kg/day. The agent in vivo inhibited the enzymatic activities of ATP-dependent citrate lyase, acetyl-CoA synthetase, cholesterol-7-alpha-hydroxylase, acyl-CoA cholesterol acyl transferase, sn-glycerol-3-phosphate acyl transferase and phosphatidylate phosphohydrolase. Tissue lipid levels of liver and small intestine also were reduced by the agent. The rat serum lipoprotein lipid content was modulated by the drug, which should be favorable for the removable of cholesterol from peripheral tissue for conduction to the liver for clearance from the body. Low density lipoprotein (LDL) cholesterol levels were reduced after treatment, which suggests that the agent potentially reduces deposition of cholesterol in plaques. If chemotherapy for atherosclerosis is to be successful, then the high density lipoprotein (HDL) cholesterol level needs to be elevated more than 16% to 25%, the level produced by current hypolipidemic agents. 2-(2,4-Dimethylphenyl)indan-1,3-dione offers a 75% increase in HDL cholesterol levels and a 30% reduction of LDL cholesterol levels with a suppression of de novo synthesis of lipids and a reduction of tissue cholesterol deposition.
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PMID:Effects of 2-(2,4-dimethylphenyl)indan-1,3-dione on serum lipoprotein and lipid metabolism of rodents. 318 7

Calcified human aortic atherosclerotic deposits and calf ventricular assist device bioprosthetic deposits were isolated and deproteinated by hydrazine treatment. Detailed chemical and instrumental analyses were applied to gain comprehensive physicochemical information which makes possible establishing compositional and structural similarities between the 2 types of pathologic mineral deposits which form on different host surfaces. These microcrystalline deposit materials are morphologically very heterogeneous and can be represented chemically as carbonate substituted apatite which, in some of its properties, significantly differs from hydroxyapatite. It is indicated that the mechanism for the formation of cardiovascular deposits proceeds through hydrolysis of octacalcium phosphate precursor.
Atherosclerosis 1988 Jan
PMID:Physiochemical characterization of cardiovascular calcified deposits. I. Isolation, purification and instrumental analysis. 328 78

Risk factors for atherosclerosis are often associated with haemorheological changes. On this point, obesity (recently advocated as an independent risk factor) was not much studied and with not univocal results. We have studied 70 obese patients (BMI greater than 30) and 50 healthy subjects (BMI less than 25). Among obese 26 had no more pathologies, 29 had hypertension, 3 suffered from ischemic heart disease, 3 suffered from occlusive arteriopathy, 9 were hyperlipidemic, 10 were smokers. We determined plasma viscosity and whole blood viscosity (at haematocrit corrected to 45% too). Washed erythrocytes, poor in leucocytes and platelets and resuspended in phosphate-buffered saline, were used for study of erythrocyte viscosity and deformability. Obese patients showed raised mean blood viscosity values when compared to healthy controls (p less than 0.01); an even more significant increase (p less than 0.001) was found concerning plasma viscosity and fibrinogen. Erythrocyte viscosity and red blood cell filterability index did not show any significant difference. We found no significant correlation between viscosity values and presence of hypertension, hyperlipidemia and smoking habit among obese. In conclusion, the higher vasculopathy incidence might be caused by an increase in blood viscosity, mostly due to plasmatic component. This fact appears to be independent from the presence of atherosclerosis complications or other risk factors.
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PMID:[Hemorrheologic disorders in obese patients. Study of the viscosity of the blood, erythrocytes, plasma, fibrinogen and the erythrocyte filtration index]. 360 Nov 35

The finding of low plasma pyridoxal-5'-phosphate levels in patients suffering from myocardial infarction has been construed as possible evidence for the pathogenetic role that vitamin B6 deficiency may play in causing premature ischaemic heart disease. However, the presence of normal plasma pyridoxal-5'-phosphate levels in patients with angiographic evidence of coronary artery narrowing but with no previous infarctions prompted the investigation of possible short-term alterations in plasma pyridoxal-5'-phosphate levels during the acute phase of myocardial infarction. In the follow-up of 30 patients with acute myocardial infarction, all of them showed a continuous decrease of approximately 45% in plasma pyridoxal-5'-phosphate levels during the acute phase. These levels subsequently returned back to normal before discharge from hospital. A large number of volunteers from an ethnic group known to have a very low incidence of ischaemic heart disease were found to have both significantly lower total cholesterol and plasma pyridoxal-5'-phosphate levels than a Caucasian group in the same geographic area which is known to have a high incidence of ischaemic heart disease. These findings therefore do not support the contention that vitamin B6 deficiency may be a risk index for ischaemic heart disease.
Atherosclerosis 1987 Feb
PMID:Vitamin B6 and coronary artery disease. Epidemiological observations and case studies. 382 84

31P-nuclear magnetic resonance spectroscopy was used to assess phosphate metabolites in perchloric acid extracts of rabbit aorta. In addition to the high energy phosphates, several other phosphorus compounds were detected and quantified. Most notable was the presence of a prominent phosphomonoester compound appearing at a chemical shift of 3.86 delta. This compound constituted 26% of the total extractable tissue phosphorus and is tentatively identified as ribose-5-phosphate, a pentose phosphate pathway intermediate. While ATP and phosphocreatine did not change during glucose and oxygen deprivation or during prolonged muscle contraction, the 3.86 delta phosphate decreased significantly. Furthermore, theophylline, an agent that increases intracellular cAMP, also decreased the level of the 3.86 delta phosphate. These results are consistent with the concept that intermediate metabolism sustains high energy phosphate pools in vascular smooth muscle in the steady state under various conditions. The pentose phosphate pathway may play an important role in vascular smooth muscle metabolism.
Atherosclerosis 1986 Jan
PMID:31P-nuclear magnetic resonance analysis of extracts of vascular smooth muscle. 394 23

Tobacco-smoking men (n = 106) showed considerably lower plasma pyridoxal-5'-phosphate levels (P less than 0.001) than non-smoking controls (n = 143). A previously reported inverse relationship between plasma pyridoxal-5'-phosphate levels and age is confirmed by using new and sensitive high-performance liquid chromatography methodology for pyridoxal-5'-phosphate determinations. Plasma pyridoxal levels were neither lower in tobacco-smoking men nor could any relationship between pyridoxal levels and age be demonstrated. Two major risk factors for coronary artery disease, tobacco-smoking and increasing age, are thus associated with lower plasma pyridoxal-5'-phosphate levels.
Atherosclerosis 1986 Mar
PMID:Depressed plasma pyridoxal-5'-phosphate levels in tobacco-smoking men. 396 55

Preliminary evidence is presented that plasma pyridoxal-5-phosphate levels are considerably and significantly reduced (P less than 0.0001) in patients suffering from myocardial infarction when compared to a healthy control group.
Atherosclerosis 1985 Jun
PMID:Plasma pyridoxal-5-phosphate level as risk index for coronary artery disease. 401 54

Myocardial biopsy specimens were taken from 10 patients undergoing aortic valve replacement using extracorporeal circulation and continuous perfusion blood cardioplegia at extremely low myocardial temperature (10 degrees C). They were analyzed for adenosine triphosphate, creatine phosphate, creatine, and lactate before, after 10 minutes, and after 60 minutes of cardioplegia. Patient inclusion criteria were heart volume less than 700 ml/m2 body surface area and no significant coronary atherosclerosis as judged from preoperative angiograms. The profound hypothermic cardioplegia resulted in a smaller intramyocardial lactate accumulation but a greater decrease in adenosine triphosphate and creatine phosphate than a moderate reduction of myocardial temperature (15 degrees C) as previously reported in a similar patient group. This suggests that at the lower temperature energy-generating processes are thwarted more than energy consumption. In addition, the profound hypothermic cardioplegia led to a reduction of the myocardial pool of total creatine, which may delay restitution of myocardial high-energy phosphate and function after cardioplegia.
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PMID:Myocardial energy depletion during profound hypothermic cardioplegia for cardiac operations. 406 39

Young male rabbits were fed semi-purified diets containing either casein or soy protein, both at a normal (0.84%, w/w) and a high (1.44%, w/w) level of dietary calcium. At the normal calcium level, casein, as compared with soy protein, increased the concentration in serum of total and free cholesterol and the ratio of free cholesterol to phospholipid. Also, casein increased the intestinal phosphate absorption and decreased the faecal fat excretion. The hypercholesterolaemic response of the rabbits on the casein diet was significantly correlated with both phosphate absorption (r = +0.744) and fat excretion (r = -0.701). The increased amount of dietary calcium inhibited the casein-specific effects on both the intestinal and the serum lipid parameters. In contrast, calcium did not change these parameters in rabbits fed the soy protein diet. These results support the hypothesis that the degree of phosphorylation of casein is involved in the mechanism of the casein-induced hypercholesterolaemia by means of its effect on the enterohepatic cycle of bile acids.
Atherosclerosis 1985 Aug
PMID:Casein-induced hypercholesterolaemia in rabbits is calcium-dependent. 407 52

Cytochrome P-450-dependent mixed function oxidase activity is present in vascular tissue; however, as far as we could determine, the distribution of monooxygenase activity across the blood vessel wall has not previously been assessed. The aryl-hydrocarbon hydroxylase activity was examined by metabolism of benzo[a]pyrene in microsomes prepared from intimal and smooth muscle cell scrapings of the hog thoracic aorta. Microsomes of intimal cells comprising 95% endothelial cells showed an approximately 2.5-fold increase in aryl-hydrocarbon hydroxylase activity compared with that in microsomes prepared from medial smooth muscle cells. Michaelis-Mentin kinetics for the intimal enzyme yielded an apparent Km value of 11.11 microM and an apparent Vmax of 3-OH benzo[a]pyrene of 40 pmol/mg protein/10 min. Aryl-hydrocarbon hydroxylase activity was dependent on nicotinamide adenine dinucleotide phosphate and was inhibited by 7,8 benzoflavone, SKF 525A, and carbon monoxide. The localization of cytochrome P-450-dependent mixed function oxidase primarily to the intimal surface of the aorta may indicate a role for this enzyme system in vasoregulation and the pathogenesis of atherosclerosis.
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PMID:Presence of cytochrome P-450-dependent monooxygenase in intimal cells of the hog aorta. 407 22


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