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

The involvement of collagen in cholesterol-induced atherosclerosis in rabbits was investigated. Rabbits were fed a 2% cholesterol diet for 8, 16, 30, 60 and 90 days. Histological sections were taken and aortic free and esterified cholesterol were determined after separation on thin-layer chromatography. Prolyl hydroxylase activity was used as a measure of collagen synthetic rate and hydroxyproline levels as an estimate of collagen content. Cholesterol content was a significantly increased after 8 days, while at this time there were no gross aortic lesions. After 30 days there was some aortic disease and by 60 days most of the rabbits exhibited pronounced aortic lesions. Histologically, the lesions consisted mainly of intimal foam cells. There was no alteration in collagen synthetic rate or content at 8, 16, 30 or 60 days. These data indicate that 60 days of continuous cholesterol feeding results in a foam cell aortic lesion with no alteration in collagen metabolism. After 90 days of cholesterol feeding there was significant increase in collagen synthetic activity in the thoracic aorta. These data suggest that alteration of collagen synthetic activity is secondary response, resulting from injury induced by the aortic accumulation of large amounts of cholesterol.
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PMID:Collagen metabolism during the early stages of cholesterol-induced atherogenesis in rabbits. 97 70

This review has highlighted some of the factors which influence the formation and fate of thrombi. Rheology and flow, the coagulation mechanism, the fibrinolytic enzyme system, and the properties of platelets to adhere and aggregate all play a significant role. Of paramount importance to neurosurgeons is the role of the vascular wall in thrombogenesis. The ulcerated atherosclerotic plaque demonstrates this point. Factors contributing to thromboembolism in this setting include stenosis and reduced flow, turbulence, and the elements in the lesion with which blood interacts. These are principally collagen, ADP, fatty acids, and the thromboplastic activity of vascular subendothelial tissue. Current concepts of the etiologies of atherosclerosis were discussed. Along with other predisposing factors, platelets may play a significant role in the initiation of the process. The current status of clinical trials with inhibitors of platelet function in the treatment of cerebrovascular disorders was reviewed. In vascular reconstructive surgery, the principles which underlie good technique are those which best insure against thrombosis. The briefest possible period of stasis during surgery should be maintained. The reconstruction should result in a smooth blood flow pattern with rapid runoff and minimal stenosis or gaps between apposed endothelial surfaces.
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PMID:Hematological and vascular concepts in relation to stroke. 97 74

Evidence from actuarial statistics, epidemiologic studies, and laboratory experiments clearly indicates that hypertension has an accelerating effect on atherogenesis, and this atherogenesis appears to be a graded function of elevated intra-arterial pressure. The fact that atherosclerosis occurs preferentially in the abdominal aorta and iliofemoral arteries seems likely to result from the pressure augmentation by reflected pulse waves that is intensified by vasoconstriction and also by the increase in hydrostatis pressure that results from gravitational stress during standing. Vasoconstriction is a characteristic of hypertension and occurs also with upright posture. The predilection of the coronary epicardial vessels for atherosclerosis seems likely to relate to subtle pressure-volume changes in these arteries as a result of this vascular bed being in the highest pressure area of the arterial system and because intramyocardial arterial branches are completely occluded during systole. The possibility is presented that hypertension accelerates atherosclerosis because it is a metabolic determinant of the multifunctional arterial smooth muscle cells which have the potential for forming collagen and mucopolysaccharides as well as phospholipid.
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PMID:The relationship of hypertension to coronary, aortic, and iliofemoral atherosclerosis. 109 12

Fibrous proteins were measured in five arterial beds in adult cynomolgus monkeys after administration of atherogenic and regression regimens. Atherosclerosis was induced by feeding the monkeys a hypercholesterolemic diet containing 1.2% cholesterol for 17 months. A low-fat, cholesterol-free regression diet was then given for 60 days, 200 days, and 20 months. In atherosclerosis, collagen concentration (mg/g dry weight) and collagen content (mg/cm length of artery) both increased. At 200 days of regression the collagen concentration, but not the collagen content, was higher than it was in atherosclerosis. In late regression (20 months), the collagen content was lower than it was in atherosclerosis, although in the five arterial beds considered together the collagen concentration was not significantly lower. Both the elastin concentration and the elastin content rose in atherosclerosis and decreased in regression. These mass data suggest that fibrous proteins are lost from the arterial wall during a regression regimen. Correlative evidence suggests that younger intimal fibers may be chiefly susceptible to fibrolytic activity, leaving dense intimal scars characteristic of regressed arteries.
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PMID:Arterial fibrous proteins in cynomolgus monkeys after atherogenic and regression diets. 111 35

Since Duguid suggested that atherosclerosis represents essentially the organization of mural thrombi, there have been many attempts to produce the disease experimentally by damaging the arterial wall. A single injury to the inner lining of an artery causes lipid-free lesions, composed of smooth muscle cells and collagen, covered by endothelium. Previously, we reported the development of atherosclerotic lesions in normolipemic rabbits as a result of repeated or continuous intimal injury by an indwelling aortic polyethylene catheter. However, it was difficult to control the location or duration of the intimal injury. The present investigation was designed to produce repeated endothelial injury in a defined segment of rabbit carotid artery. Sixty-two rabbits received injections of either lymphocytotoxic-positive (LP) or lymphocytotoxic-negative (LN) human serum into a segment of left carotid artery. Autologous rabbit serum was injected into the right carotid artery as a control. Eight rabbits received a single injection of LP and were killed 4 weeks latermforty-two rabbits received injections of human serum at weekly intervals, for a maximum of four injections, and were killed 1 week after the last injectionmthirty-two of 42 rabbits received repeated injections of LP; 10 received repeated injections of LN. Raised, lipid-containing lesions were present in 21 of 26 rabbits receiving four repeated injections of LP. No, or very minimal (fewer than three cells thick), intimal thickening was found in the 10 LN rabbits and in all control right carotid arteries. In eight rabbits receiving one injection of LP, fibrous intimal thickening without lipid accumulation, fatty streaks, and edematous plaques were found. Electron microscopy of arteries from 12 rabbits sampled at 1,5, and 60 minutes after exposure to LP indicated that the initial damage was loss of endotheliummthe results consistently showed lipid in raised, thrombus-covered (non-reendothelialized) lesions. Nonraised, endothelialized lesions did not show lipid. These findings support the belief that atherosclerosis occurs in response to repeated endothelial injury.
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PMID:Repeated endothelial injury and induction of atherosclerosis in normolipemic rabbits by human serum. 112 16

The effect of hyperlipidemic rat serum and its fractions on the synthetic functions of embryonic fibroblasts was studied. Moderately hypercholesterolemic sera (100-140 mg/100 ml) stimulated the synthesis of collagen, but not the synthesis of non-collagenous proteins nor the incorporation of glucosamine or cytidine. The stimulating principle was nondialyzable. It was not associated with the isolated total lipoproteins but was found in the infranatant fraction of sera centrifuged at a density of 1.220.
Atherosclerosis
PMID:Effect of hyperlipidemic rat serum on the synthesis of collagen by chick embryo fibroblasts. 114 29

The selectively-bred substrains of spontaneously hypertensive rats with a greater vulnerability to vascular lesions rapidly developed arterial fat deposition within 1 or 2 weeks as well as a greater hypercholesterolemic response when fed on high fat cholesterol diet including 20% of suet, 5% of cholesterol and 2% of cholic acid. The ring-like arterial fat deposition at the branches of superior mesenteric arteries and cerebrobasal arteries, which was found to be good indices for the deposition of intrarenal or coronary arteries, was not observed in normotensive rats fed on high fat cholesterol diet for 3 months, greatly delayed in SHR under antihypertensive treatment and accelerated by 1% salt loading in drinking water. The horseradish peroxidase infused intravenously 1 to 4 hours before sacrifice leaked in ring-like forms which corresponded to the fat deposit in mesenteric arteries. The incorporation of 3H-proline infused 4 hours before sacrifice was enhanced in the mesenteric arteries with the fat deposition. These results clearly indicated that hypertension was a great contributory factor to rapid arterial fat deposition, which was caused by an increased vascular permeability and enhanced the arterial collagen formation, the initiation process of arterio- or atherosclerosis.
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PMID:Pathogenesis of acute arterial fat deposition in spontaneously hypertensive rats. 115 92

Apoproteins from plasma lipoproteins were localized by immunofluorescence techniques in human carotid artery atherosclerotic lesions. These studies were performed in light of the possible importance of these apoproteins in both lipid metabolism and the pathogenesis of atherosclerosis. ApoA-I from high density lipoproteins, apoB from low density lipoproteins, and apoC-III from very low density lipoproteins were localized also as markers for their respective lipoproteins, since the latter cross-react immunologically. The three apoproteins were localized to the same regions of lesions as neutral lipids and, to some extent, fibrinogen. These regions consisted of bands of collagen fibers, usually deeper within the lesion, and the lipid core or atheroma of such advanced lesions. Although the superposition of localization for the three apoproteins and lipid was only 53%, it was suggested that deviation from complete superposition was due to the abrupt changes in lesion structure resulting from the focal nature of the atherosclerotic process. These results suggest that there is a broader specificity than previously implied of the interaction between such lesion components as connective tissue and extracellular lipid accumulations, and apoproteins from plasma lipoproteins. This interaction is believed to result in a net retention within atherosclerotic lesions of human extracranial arteries of these plasma-derived factors, either as free apoproteins or as native lipoproteins.
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PMID:Localization of apo-lipoproteins in human carotid artery plaques. 117 63

The relation of lactation and weaning to the development of early arterial lesions in the female breeder rat was investigated. Changes in aortic hexosamine and 35S-uptake, which are indicative of ground substance metabolism were correlated with changes in aortic calcium, phosphorus, and 45Ca-uptake during lactation and weaning. Lactation was associated with reduced aortic hexosamine content and lowered uptake of [S]sulfate. Further dynamic changes in aortic metabolism of these substances occurred following weaning in conjunction with an intense calcium uptake in the aorta of some, but not all, of the post-lactation animals. These latter changes were associated with the beginning aortic calcifications. Histopathologically, early arterial lesions developing during lactation, consist of intimal accumulations of mucopolysaccharide capped over by collagen. With repeated breeding cycles, these early lesions become exacerbated with extensive medial calcification occurring in areas rich in mucopolysaccharide and collagen particularly around degenerating elastic fibers. The hormones associated with reproduction and lactation may have a conditioning effect on these arterial connective tissue alterations and the development of arterial degenerative changes.
Atherosclerosis
PMID:Aortic hexosamine, [35S]sulfate uptake, and calcium metabolism related to early arterial degenerative changes induced by lactation and forced weaning in breeder rats. 119 74

(1) Annulus fibrosus and nucleus pulposus of human intervertebral discs at different degrees of atherosclerosis were disintegrated by elastase. (2) The material disintegrated by elastase -- called elastolysate -- could be separated into hydrophobic (apolar) and hydrophilic (polar) peptides. Parallel with the degree of atherosclerosis the amount of hydrophobic peptides increased, whereas that of the hydrophilic peptides decreased. (3) In annulus fibrosus and nucleus pulposus two kinds of fluorescence maxima were measured. The one, A:F 350:405, is known as fluorescence maxima of elastin- and collagen-peptides. The other, A:F 410:470, is related to a similar substance called atherofluorescent component (AFC), which has been isolated before from the plaques of atherosclerotic aorta. This substance accumulates mainly in nucleus pulposus and resembles lipofuscin-like bodies. (4) These bodies show a positive reaction with thiobarbituric acid, giving a red coloration characteristic for malondialdehyde. In nucleus pulposus the amount of lipofuscin-like substances is much greater than in annulus fibrosus. (5) The hydrophilic peptides, although they show the same fluorescence maxima as the hydrophobic peptides, do not give any reaction with thiobarbituric acid. It is supposed that in these cases the cross-linked protein contains instead of malondialdehyde other reactive aldehydes.
Atherosclerosis
PMID:Investigations of fluorescent peptides and lipofuscins of human intervertebral disc relating to atherosclerosis. 120 Nov 51


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