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)

Ischemic optic neuropathy and retinal arterial occlusion are 2 forms of arterial occlusive disease affecting the eye. Reports in the literature suggest platelet hyperactivity in acute arterial occlusive diseases affecting other organ systems. Therefore, 14 patients with ischemic optic neuropathy and 17 patients with central or branch retinal artery occlusion were studied to determine whether platelets have a role in the pathogenesis of these vascular occlusive disorders. The results of the following investigations were no different in these patients compared with those in 18 control patients with non-vascular eye diseases: prothrombin times, partial thromboplastin times, plasma fibrinogen, factor V, factor VIII, platelet counts and threshold concentrations of ADP, epinephrine and collagen resulting in secondary platelet aggregation and serotonin release. In contrast, platelet coagulant activities concerned with the early stages of intrinsic coagulation were significantly increased in patients with retinal artery occlusion without hypertension or type IV hyperlipoproteinemia, but generally normal in patients with ischemic optic neuropathy and in patients with retinal artery occlusion associated with hypertension, type IV hyperlipoproteinemia, diabetes mellitus and generalized atherosclerosis. These results are consistent with a platelet contribution to retinal arterial occlusive disease in patients without other known contributing factors such as hypertension, serum lipid abnormalities, diabetes mellitus and generalized atherosclerosis and may have implications regarding prophylaxis.
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PMID:Platelet coagulant activities in arterial occlusive disease of the eye. 50 1

Segments of human thoracic aorta were maintained in long-term explant culture for 18 weeks in serum-supplemented medium. The aortas were grossly normal in appearance, and random samples fixed for light microscopy prior to culture revealed a normal morphology. The intima contained no more than five layers of smooth muscle cells. After 7 days in culture, the intima was noticeably thicker than the uncultured segments. The increased thickness was due to proliferating smooth muscle cells and production of extracellular material. After several months in culture, extracellular material consisting of collagen and flocculent material was present in areas resembling atherosclerotic fibrous plaques. A peripheral growth, which formed around the explant, was composed of fibroblastlike cells and added to the overall thickness of the intima. However, aortic segment maintained for up to 2 months in serum-free culture medium showed no cellular proliferation. This study demonstrates that changes resembling early stages of atherosclerosis occur in human aortas maintained in explant culture using routine culture procedures.
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PMID:Long-term culture of human aortas. Development of atherosclerotic-like plaques in serum-supplemented medium. 53 10

Although glycosaminoglycans, particularly proteoglycans, have been characterized biochemically in normal and diseased arteries, little is known regarding their ultrastructural characteristics in human arteries. The observations reported here were made in renal arteries from nephrectomy specimens from patients with endstage kidney disease and hypertension. By light microscopy, the diffusely thick intima is characterized by small, slender smooth muscle cells embedded in a finely fibrillar, strongly alcian-blue positive, intercellular matrix. Ultrastructurally, there is a loose meshwork of collagen fibrils, elastic units and abundant fibrillogranular units staining strongly with ruthenium red and identified as proteoglycans. These consist of ovoid or diamond-shaped electron-dense granules about 300-500 A in diameter, having fine filamentous processes.
Atherosclerosis 1977 Oct
PMID:Ultrastructure of proteoglycans in human renal arteries from end stage renal disease. 56 69

Individuals with familial hyperbetalipoproteinemia are at increased risk of premature atherosclerosis and thrombosis. Although there is controversy whether platelet survival is shortened or normal in this disease, several in vitro tests of platelet function are abnormal including a decreased threshold concentration for stimulation of aggregation by ADP, epinephrine and collagen and increased release of nucleotides to the same agents. These functional changes are accompanied by an increase of cholesterol to phospholipid ratio in the platelet membrane and in low density lipoprotein in individuals with type IIa hyperlipoproteinemia. Clofibrate and halofenate reverse some of the abnormalities in vitro and the former drug, when administered for 6 weeks to patients with type IIa hyperlipoproteinemia decreases platelet sensitivity to ADP and epinephrine. The platelet hypersensitivity to aggregating agents can be reproduced in vitro by increasing the cholesterol to phospholipid rather in normal platelets. These artificially hypersensitive platelets can be returned to normal by halofenate in vitro. Incorporation of cholesterol into platelet membranes increases the basal level of the membrane associated enzyme adenylate cyclase. However, the enzyme no longer responds to stimulation by prostaglandin E1, and this is associated with relative resistance of the platelet to inhibition by this pharmacologic agent. These functional alterations produced by cholesterol enrichment of platelet membranes occur is parallel with an increase in platelet membrane microviscosity suggesting that the more rigid membrane can alter the behavior of membrane associated enzymes and receptors. A correlation appears to exist between the ability of certain drugs to induce phase separation in model membranes and the potency in inhibitory platelet aggregation.
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PMID:Platelet function in hyperbetalipoproteinemia. 58 Sep 82

Human coronary arteries with various degrees of atherosclerosis were analyzed for the concentration of different types of glycosaminoglycans (GAGs). The changes in GAGs were considered against the background of macroscopic atherosclerosis, and the concentration of glycoprotein-bound hexosamines, collagen, calcium and cholesterol. The concentration of calcium was increased and that of hyaluronic acid decreased even in mildly atherosclerotic coronary arteries. The additional changes in advanced atherosclerosis included the increase of collagen and dermatan sulphate and the decrease of heparan sulphate. Cholesterol was increased in mild, and even further in advanced, atheroslcerosis. The concentrations of chondroitin sulphates and glycoprotein-bound hexosamines were not significantly affected by atherosclerosis.
Atherosclerosis 1978 Feb
PMID:Connective tissue components in normal and atherosclerotic human coronary arteries. 64 48

Microangiopathy is a more or less pronounced PAS deposit-located exterior to the endothelial cells of the lymphatics and the basal membrane of the capillaries. This lesion, found in various normal and pathological states, has generated numerous pathogenic hypotheses. The presence of microangiopathy in 5 groups of 50 subjects representing five different clinical conditions, subjects over 60 years old or less than 40, diabetics, latent diabetics or patients with severe coronary heart disease, together with microscopic and/or ultrastructural lesions of the connective tissue (fibroblasts, collagen and elastic fibers, ground substance) has enabled us to propose a pathogenic hypothesis applicable to any microangiopathy. The initial change, hereditary or acquired, would be fibroblastic or interstitial. It would be characterized by the accumulation of glycoproteins, proteoglyacans and soluble collagen in the interstitium. Incomplete drainage of these macromolecules would occur around the blood and lymphatic capillaries and manifest itself by a PAS deposit, the hallmark of the microangiopathy.
Atherosclerosis 1978 Mar
PMID:Hypothesis on microangiopathy of cutaneous capillaries. 66 87

In 6 healthy adults the effect of essential oil of garlic on platelet aggregation was studied in vitro with an aggreganometer. The blood was collected in a siliconized centrifuge tube containing sodium citrate. The aggregating agents used were ADP, epinephrine and collagen. In each subject aggregation was studied 3 times: (i) initial fasting control; (ii) immediately after (i) but with essential oil of garlic drawn into the syringe together with the sodium citrate; (iii) 5 days after feeding 0.5 mg of essential oil of garlic daily. Addition of essential oil of garlic inhibited in-vitro platelet aggregation induced by ADP, epinephrine or collagen; the effect was dose-related. Oral administration of garlic also decreased platelet aggregation. Thus, garlic seems to inhibit some aspects of thrombus formation.
Atherosclerosis 1978 Aug
PMID:Effect of garlic on human platelet aggregation in vitro. 70 92

A possibility is shown of obtaining sufficiently pure antigens (collagen, elastin, structural grycoproteids), with the help of a preparative chemical method, from the wall of aortas of rabbits, both healthy and "diseased", i.e. with atherosclerosis. Immunomorphological analysis showed that the immune sera obtained against antigens indicated above reacted only with structures of the affected vessels, no interaction with the wall of normal aortas being noted.
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PMID:[Isolation of immune serums against antigens of the aorta for immunomorphological study of experimental atherosclerosis]. 77 46

Rats were made hypercholesterolemic by feeding them a high-cholesterol, olive oil diet for one week. The effect of sera and 35,000 X g supernatants of liver homogenates on collagen synthesis was studied in isolated aortas, cultured arterial smooth muscle cells and the same cells in suspension. Compared to the preparations from normal rats, the liver preparations from hyperlipidemic rats stimulated collagen synthesis in both isolated aortas and cultured smooth muscle cells by about 25%. In these test systems hyperlipidemic serum was without effect but when added to smooth muscle cells incubated in suspension, produced a significant increase in the amount of collagen secreted. Hyperlipidemic serum caused an increase of about 50% in the incorporation of [3H]-thymidine by cultured smooth muscle cells.
Atherosclerosis 1977 Mar
PMID:Effect of serum and liver extracts from hypercholesterolemic rats on the synthesis of collagen by isolated aortas and cultured aortic smooth muscle cells. 84 73

Atherosclerotic segments of pigeon aorta synthesized collagen at four times the rate found in normal aorta (Athero = 2071 +/- 1339 ng/g/h; Control = 497 +/- 192 ng/g/h; P less than 0.025). Similar results were obtained when synthesis was expressed per mg DNA. Elevation in collagen synthesis was relatively specific, collagen accounting for 4% of total protein synthesis in lesion-free aorta and 11.5% in atherosclerotic aorta. Substantial increases in total collagen were observed in atherosclerotic aortas (Athero = 9.9 +/- 3.1 mg/aorta; Control = 6.0 +/- 1.3 mg/aorta; P less than 0.05). Ultrastructural studies revealed the accumulation of large amounts of dense fibrillar collagen in the sub-endothelial region of the plaque. Plaque cells contained multiple vacuoles, an extensive rought endoplasmic reticulum and many mitochondria, suggesting active protein synthesis. It is concluded that increased collagen biosynthesis and deposition is an important metabolic derangement in lipid-rich atherosclerotic lesions whihc promotes their gradual conversion to fibrous plaques.
Atherosclerosis 1977 Mar
PMID:Enhanced synthesis and accumulation of collagen in cholesterol-aggravated pigeon atherosclerosis. 84 79


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