Change in endothelial cell morphology at arterial branch sites caused by a reduction of intramural stress

Baker, Joseph W.; Thubrikar, Mano J.; Parekh, Jayashree S.; Forbes, Michael S.; Nolan, Stanton P.

doi:10.1016/0021-9150(91)90062-8

Cited by 22 publications

(9 citation statements)

References 25 publications

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“…In fact, the cells of the proximal aorta of these animals showed a rounded shape as well as intercellular junction alterations. These changes could be due to local mechanical forces such as intramural stress and shear stress that can affect the atherosclerosis-prone vessels such the proximal aorta [5,6]. In addition, endothelial cells presented edema and lipid inclusions.…”

Section: Discussionmentioning

confidence: 98%

“…These permeability changes might be due to high plasma lipids, since it has been shown that exposure of endothelial cells to lipids causes membrane fluidity alterations [1], although an intramural stress increase in the vascular wall has also been suggested [5]. In addition, oxidized LDL can further induce changes in endothelial cell function [39].…”

Section: Discussionmentioning

confidence: 99%

“…Intimal thickening, mainly as a consequence of macrophage-derived foam cell accumulation, is the main feature of atherosclerotic lesion, although smooth muscle cells also contribute to the lesion through cell accumulation and extracellular matrix production [8,33]. Changes in endothelial and smooth muscle cell ultrastructure have also been associated with atherosclerosis [5,6].…”

Section: Introductionmentioning

confidence: 99%

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The protective role of atorvastatin on function, structure and ultrastructure in the aorta of dyslipidemic rabbits

et al. 2000

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Responses to both an endothelium-dependent (acetylcholine 10(-9)-10(-5) mol/l) and an endothelium-independent vasodilator (sodium nitroprusside 10(-10)-10(-6) mol/l) were studied in aortic rings from rabbits fed or not with a diet containing 0.5% cholesterol plus 14% coconut oil for 14 weeks and treated or not with atorvastatin (2.5 mg/kg/day). Morphometric and ultrastructure analyses were also performed. Rabbits fed the dyslipidemic diet presented higher plasma cholesterol and triglyceride concentrations than controls (P < 0.05). This was associated with intima-media thickening and, consequently, aortic stenosis (29 +/- 3%) since vessel cross-sectional area did not change. Endothelial cells presented numerous alterations in dyslipidemic rabbits. Atorvastatin treatment only reduced plasma levels in dyslipidemic rabbits (P < 0.05), which were nevertheless higher than those of controls. In addition, it prevented the reduction in acetylcholine relaxation in hypercholesterolemic animals. Atorvastatin administration also enhanced the response to acetylcholine in rabbits fed a control diet. Likewise, atorvastatin treatment reduced lesion area and consequently increased aortic lumen in dyslipidemic rabbits but did not modify media thickening. It also prevented the majority of the ultrastructural changes observed in endothelial cells. In conclusion, chronic atorvastatin treatment exerts a protective role in vascular function, structure and ultrastructure even in the presence of high cholesterol and triglyceride plasma levels.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The protective role of atorvastatin on function, structure and ultrastructure in the aorta of dyslipidemic rabbits

et al. 2000

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“…It may be that reduced cyclic stretch of the vessel wall during the cardiac cycle inhibits the uptake of cholesterol, lipoproteins, and other molecules 23 and that endothelial cell adhesion may be reduced. 9 External wrapping of any vessel reduces wall stress, which may alter endothelial cell structure and function 24 or induce endothelial cell enzymes or autocrine factors. 25,26 An inflammatory reaction between the adventitia and external wrap is probably formed, and it may also be responsible for reduced intimal proliferation.…”

Section: Discussionmentioning

confidence: 99%

Reduction of Aortic Wall Motion Inhibits Hypertension-Mediated Experimental Atherosclerosis

Tropea

Schwarzacher

Chang

et al. 2000

ATVB

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Abstract-Hypertension is a well-known risk factor for coronary artery disease and carotid and lower extremity occlusive disease. Surgically induced hypertension in hypercholesterolemic animals results in increased aortic wall motion and increased plaque formation. We tested the hypothesis that reduction in aortic wall motion, despite continued hypertension, could reduce plaque formation. New Zealand White rabbits (nϭ26) underwent thoracic aortic banding to induce hypertension and were fed an atherogenic diet for 3 weeks. In 13 rabbits, a segment of aorta proximal to an aortic band was externally wrapped to reduce wall motion. All animals were fed an atherogenic diet for 3 weeks. Four groups were studied: 1, coarctation control (no wrap, nϭ7); 2, coarctation with loose wrap (nϭ6); 3, coarctation with firm wrap (nϭ7); and 4, control (noncoarcted, nϭ6). Wall motion, blood pressure, and pulse pressure were measured at standard reference sites proximal and distal to the coarctation by use of intravascular ultrasound. Quantitative morphometry was used to measure intimal plaque. Mean arterial pressure and cyclic aortic wall motion were equally increased proximal to the aortic coarctation in all 3 coarcted rabbit groups compared with the control group (PϽ0.001). Wall motion in the segment of aorta under the loose and firm wraps was no different from the control value. The external wrap significantly reduced intimal thickening in the 4 groups by the following amounts: group 1, 0.30Ϯ0.03 mm 2 ; group 2, 0.06Ϯ0.02 mm 2 ; group 3, 0.04Ϯ0.02 mm 2 ; and group 4, 0.01Ϯ0.01 mm 2 (PϽ0.001). Localized inhibition of aortic wall motion in the lesion-prone hypertensive aorta resulted in significant reduction in intimal plaque formation. These data suggest that arterial wall cyclic motion may stimulate cellular proliferation and lipid uptake in experimental atherosclerosis. Key Words: wall motion Ⅲ hypertension Ⅲ atherosclerosis Ⅲ pulse pressure H ypertension is an independent risk factor for coronary artery disease 1,2 and for carotid 3,4 and lower extremity 5,6 occlusive disease. Other multivariate clinical studies have shown that pulse pressure is also an independent risk factor for atherosclerosis. 7,8 Previous experimental studies in our laboratory 9,10 and in others 11,12 have demonstrated that surgically created aortic coarctations increase blood pressure proximal to the coarctation and increase the rate of plaque deposition in hypercholesterolemic rabbits and monkeys.On the other hand, the aorta distal to a severe coarctation experiences reduced wall motion and is largely protected from plaque formation despite hypercholesterolemia in animals. 13 In a separate study, rigid external casts of lesion-prone arteries in normotensive hypercholesterolemic rabbits inhibited plaque formation, perhaps because of reduced wall motion. 14 In the present experiment, we reduced aortic wall motion in the hypertensive atherosclerosis-prone aorta proximal to a coarctation by externally wrapping a segment of aorta and studied the effect on plaq...

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“…[31][32][33][34][35] In vivo studies have shown that at major artery branching points, where both turbulent flow and jet flow are present, endothelial cells are spindle-shaped with disrupted borders or cobblestone-shaped and disoriented with respect to the direction of flow. 36 Endothelial nuclei impressions located near a branch that could be affected by complicated local flow conditions were therefore excluded from the study. In Eng ϩ/Ϫ mice, endothelial nuclei were rounder and had a more irregular orientation, indicative of local reduction in shear stress or turbulent flow and consistent with increased incidence of relative dilatation and abnormal arteriolar structure.…”

Section: Discussionmentioning

confidence: 99%

Cerebral Vascular Abnormalities in a Murine Model of Hereditary Hemorrhagic Telangiectasia

Satomi

Mount

Toporsian

et al. 2003

Stroke

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Background and Purpose-Hereditary hemorrhagic telangiectasia type 1 (HHT1) is an autosomal dominant vascular dysplasia caused by mutations in the endoglin gene and characterized by dilated vessels and arteriovenous malformations (AVMs). To understand the etiology of this disorder, we evaluated the cerebral vasculature of endoglin heterozygous (Eng ϩ/Ϫ ) mice, which represent the only animal model of HHT1. Methods-The cerebral vasculature of Eng ϩ/Ϫ and Eng ϩ/ϩ mice from C57BL/6 (B6) and 129/Ola (129) strains with a differential susceptibility to HHT1 was studied with corrosion casting. Casts were observed by scanning electron microscopy to detect malformations and evaluate arterial diameters and orientation of endothelial nuclei. Measurements were taken to assess relative constriction at arteriolar branching points and downstream relative dilatation. Results-Three of 10 Engϩ/Ϫ mice demonstrated abnormal vascular findings including AVMs, while none of 15 Eng

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Change in endothelial cell morphology at arterial branch sites caused by a reduction of intramural stress

Cited by 22 publications

References 25 publications

The protective role of atorvastatin on function, structure and ultrastructure in the aorta of dyslipidemic rabbits

The protective role of atorvastatin on function, structure and ultrastructure in the aorta of dyslipidemic rabbits

Reduction of Aortic Wall Motion Inhibits Hypertension-Mediated Experimental Atherosclerosis

Cerebral Vascular Abnormalities in a Murine Model of Hereditary Hemorrhagic Telangiectasia

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