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

The typical occupational cohort study includes all causes of mortality. However, emphasis is usually placed on the presence or absence of excess cancer mortality. A systematic review of completed occupational cohort studies to assess the findings and patterns of cardiovascular mortality would be useful. Although many of these studies will illustrate the "healthy worker effect" with deficits in mortality, particularly from cardiovascular causes, a thorough review should indicate certain exposures needing further research. A recently published study of heart disease mortality in the rubber industry illustrates the potential use of such a literature review with subsequent follow up. Production workers in the rubber industry have shown small excesses in CAHD mortality. A follow-up study at one plant confirmed the known association between carbon disulfide and atherosclerosis, as well as suggested two new causal associations between CAHD and the use of phenol and ethanol as solvents. What additional techniques can be used to generate hypotheses on heart disease and occupation? Some possibilities include: A recent article describes the use of the results of occupational disease surveillance systems for occupational cancer research. A review of such systems for heart disease would be equally useful. It would be useful to review the quality and quantity of occupational data that has been collected in prospective cohort studies, such as those in Framingham and Evans County. The importance of examining the association between occupational exposures and heart disease include: Assessing whether adequate protection is afforded by current limits on exposure to substances known to cause heart disease (carbon disulfide, nitrates, and carbon monoxide).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular disease and work place exposures. 638 Apr 27

The thoracic aortas from two rabbits that had survived a single embolectomy catheter lesion for 2 years were studied by transmission electron microscopy after vital staining with Evans blue. An intimal thickening was formed inside the original internal elastic lamella in the re-endothelialized areas. Small blue areas in the ventral aortic wall showed intact endothelial cells covering an amorphous structureless subendothelial matrix. These observations indicate that endothelial cells do not form an effective barrier in the absence of differentiated subendothelial connective tissue.
Atherosclerosis 1983 Sep
PMID:The importance of the subendothelial connective tissue to the permeability of the neointimal barrier. 663 8

Whereas squirrel monkeys have an inherent susceptibility to atherosclerosis, cebus monkeys are relatively resistant. To assess whether this difference might lie in their response to endothelial injury, the acute morphologic changes in the aortic intima after endothelial removal were examined in the two species. The endothelium of the lower thoracic aorta was removed with an embolectomy catheter, and the intimal response was compared with the uninjured upper thoracic aorta in each monkey. By 21 days after aortic denudation, regrowth of the endothelium (assessed by in vivo Evans' blue dye staining) was significantly greater in squirrel monkeys (90% +/- 5% of aortic surface) than in cebus (56% +/- 11%). Squirrel monkeys had comparable sudanophilic surface in the nonballooned, control aorta (25% +/- 7%) and the ballooned, lower thoracic segment (17% +/- 6%). Cebus monkey aortas had no sudanophilia in either segment. The intima/media ratios (IMR) in all regions of the aorta were significantly greater in squirrel monkeys than in cebus, but in both species the IMR of the ventral ballooned segment was two to three times the IMR of the nonballooned control segment. In the dorsal aorta, where endothelial regrowth was more rapid, the IMR was similar to the control aortic segment. By electron microscopy the thickened aortic intima in both species contained a marked increase in modified smooth muscle cells, but lipid accumulation did not result from endothelial removal or regrowth in either species. Thus, although the squirrel monkey aorta had atherosclerotic lesions before endothelial removal, the acute intimal response to endothelial injury was similar in degree and kind in both cebus and squirrel monkeys. This suggests that factors other than those controlling the initial intimal thickening following endothelial injury are responsible for the observed difference in arterial lipid accumulation between cebus and squirrel monkeys.
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PMID:Aortic intimal response to endothelial removal in cebus and squirrel monkeys. 670 51

Accumulation of arterial platelets was calculated from 51Cr radioactivity in the intima-inner media of flushed, perfuse-fixed aortas and branch vessels of cynomolgus monkeys 48 hours after labeling of the blood platelets. In normo-cholesterolemic controls the radioactivity per square centimeter of tissue was consistently higher in aortic branching sites (circumostial aorta) than in the remainder of the aorta. In monkeys given 10 and 100 days of hypercholesterolemic diet radioactivity rose in circumostial aorta in proportion to increases in streaks and in areas of Evans blue uptake. In branch artery inner wall, where intimal changes were minimal and usually absent, counts were significantly greater in animals given 100 days of hypercholesterolemic diet than in controls. After 10 days of hypercholesterolemic diet the mean radioactivity in aortic branch artery inner wall uniformly exceeded control values, but usually nonsignificantly, permitting the speculation that changes in platelet-intima interactions may occur in widespread fashion throughout the arterial tree very early in hypercholesterolemia when lesion formation is incipient or absent.
Atherosclerosis 1980 May
PMID:Arterial platelet accumulation in experimental hypercholesterolemia. 677 Aug 78

A two-part study concerned the accumulation of intravenously injected Evans blue dye in the abdominal aorta of swine. In normolipidemic swine weighing up to 90 kg each, Evans blue accumulated predominantly in areas of the aorta that were the site of intimal smooth muscle cell collections. The second part of the study dealt with Evans blue accumulation in swine with advanced atherosclerosis. The extent of blue staining in these animals was not significantly different than in normolipidemic, nonatherosclerotic swine of the same size. The dye showed a predilection for raised atherosclerotic lesions, but only one quarter of the surface of these lesions was stained. Histologic studies of the uppermost portion of blue and nonblue lesion areas showed that the dye preferentially accumulated in regions with lower concentrations of foam cells. Injected isotopic cholesterol tended to accumulate in the blue rather than the nonblue areas.
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PMID:Evans blue dye. Accumulation in swine aortic intimal cell collections and atherosclerotic lesions. 689 58

Age is a risk factor in the development of atherosclerosis. In this study we investigated the hypothesis that proliferation of vascular smooth muscle cells (SMCs), an integral part of atherosclerotic plaque formation, changes with age. SMC growth kinetics of old rats (21-24 months) were compared to those of young adult rats (3-4 months). Rat aortas were denuded of their endothelium and the animals were killed after [3H]thymidine and Evans blue injections at 0-28 days after denudation. Incorporation of [3H]thymidine into SMC peaked in the young animals by day 2, whereas the older animals responded to endothelial removal with greater incorporation at day 2 and a more sustained rate of incorporation peaking at day 4. The [3H]thymidine incorporation curves decreased sharply from their peaks at 2 and 4 days, respectively, and paralleled each other after day 7. [3H]Thymidine uptake reflected the subsequent SMC intimal growth as measured morphometrically, with old animals showing greater numbers of intimal SMC than did the younger animals. The difference in response of SMC to injury with age suggests that aging produces a change in the vascular SMC that enhances proliferation. This change in response implies that the more pronounced atherosclerotic plaque growth seen with aging may be a result of an age-related increase in response to injury rather than merely the accumulation of time-related intimal change.
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PMID:Vascular smooth muscle cell growth kinetics in vivo in aged rats. 695 28

In order to investigate the effect of diazepam in reducing the incidence and severity of cholesterol induced atherosclerosis in rabbits, 3 treatment groups were compared. The control Group I received the laboratory diet alone. Group II received cholesterol (1 gm daily, given by syringe). Animals in Group III additionally received diazepam (3 mg/kg/day) orally, again by syringe. After 21 days, animals were injected with Evans blue and 3 hours later their aortas were removed and examined for permeability changes. Serum was assayed for various lipid and lipoprotein components. Cholesterol feeding produced a 10-fold increase in serum cholesterol values in Groups II and III compared to the control Group I. The aortic uptake of Evans blue was significantly increased in animals treated with cholesterol but not in those which simultaneously received diazepam. Thus, diazepam prevented the increased endothelial permeability produced by hypercholesterolaemia, but it is not yet clear whether this effect involves the central nervous system or is a consequence of some more local membrane stabilizing action.
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PMID:Effect of diazepam on endothelial permeability, plasma lipids and lipoproteins in cholesterol fed rabbits. 695 82

Following injections of Evans blue (1-200 mg/kg) into rabbits, polyacrylamide gel disc electrophoresis showed that Evans blue binds to two protein fractions. The greater part was bound to albumin and the remainder to a plasma protein in the postalbumin fraction. Unbound Evans blue was present in each plasma sample analyzed. Attempts to liberate the dye from the coloured areas of the aorta and common carotid arteries by tissue electrophoresis failed unless very high concentrations of Evans blue were used. This indicates that at the concentrations used by many investigators areas dyed by Evans blue may not be equated with the presence of diffusible protein-dye complexes.
Atherosclerosis 1982 Jun
PMID:Binding properties of circulating Evans blue in rabbits as determined by disc electrophoresis. 711 70

Aspirin and dipyridamole have been used to treat the thromboembolic complications of atherosclerosis. We studied the effects of these drugs on the rate of endothelial healing after a standard de-endothelializing injury of the thoracic aorta. Twenty-five rabbits received 13.5 mg/kg/day of aspirin and 15 mg/kg/day of dipyridamole one week before injury and for the period of endothelial regrowth. There were 25 control animals. Mean serum aspirin salicylate levels were 12 micrograms/dL at the time of injury and 15 micrograms/dL at death. Areas of endothelial regrowth were measured by Evans blue dye at 1, 4, 7 and 14 days after injury. The percentage of endothelial regrowth was measured by computer-assisted morphometry. Antiplatelet treatment retarded endothelial regrowth by 66% at four days, 22% at seven days, and 28% at 14 days. Antiplatelet drugs must be used cautiously, as re-endothelialization of injured arteries is retarded.
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PMID:Aspirin and dipyridamole inhibit endothelial healing. 713 4

Although hypertension has been identified as a risk factor in atherosclerosis, how hypertension enhances plaque growth is not clear. To study the influence of essential hypertension on injury-induced arterial intimal thickening, we employed a model of arterial endothelial injury (aortic balloon injury) in spontaneously hypertensive rats (SHR). SHR rendered normotensive with drugs served as controls. The injured vessels were fixed by perfusion at intervals between 2 weeks and 3 months and studied by light, transmission, and scanning electron microscopy. Endothelial regeneration at 2 weeks was assessed by the difference between total and blue-stained arterial surface area in rats receiving Evans blue by injection and was decreased in SHR. Intimal thickening was increased in SHR as compared with controls at all time intervals and appeared to be due to increased smooth muscle cell proliferation. Although neither SHR or controls injured arteries were stained by Evans blue at 3 months, the SHR (but not the control) injured arteries demonstrated subendothelial edema and focal necrosis in the intima. These data in a model of arterial endothelial injury support the concept that essential hypertension has a deleterious effect on arterial wound healing by enhancing arterial myointimal thickening. This effect can be reduced by adequate control of the hypertension with drugs.
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PMID:The influence of hypertension on injury-induced myointimal thickening. 739 6


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