Aortic Alterations in Rabbits Following Sheathing with Silastic and Polyethylene Tubes

Huth, F; Kojimahara, Masayasu; Franken, Tobias; Rhedin, P.; Ka, Rosenbauer

doi:10.1007/978-3-642-66215-7_1

Cited by 8 publications

(4 citation statements)

References 23 publications

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“…17 Huth et al 22 speculated that medial and adventitial hypoxia induced by closing of the vasa vasorum triggered the atherosclerotic process in this model. The exact mechanism of intimal thickening in this model remains unclear.…”

Section: Discussionmentioning

confidence: 86%

Thermal Treatment Attenuates Neointimal Thickening With Enhanced Expression of Heat-Shock Protein 72 and Suppression of Oxidative Stress

et al. 2004

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Background-The beneficial effects of thermal therapy have been reported in several cardiovascular diseases. However, it is unknown whether the thermal treatment has some beneficial roles against the development of atherosclerosis. Methods and Results-The inflammatory arterial lesion was introduced by placement of a polyethylene cuff on femoral arteries of male Sprague-Dawley rats for 4 weeks. Thermal-treated group underwent daily bathing in 41°C hot water for 15 minutes. Neointimal thickening along with immunohistochemical expression of heat-shock proteins (HSPs), monocyte chemoattractant protein-1 (MCP-1), and NADPH oxidase were compared with those of a thermally untreated (Control) group. Morphometric analysis demonstrated a significant suppression of neointimal thickening in thermal-treated group compared with the Control group (intimal/medial area ratios, 0.01Ϯ0.01 versus 0.31Ϯ0.04, PϽ0.01). Expression of MCP-1 and infiltration of ED-positive cells were enhanced in the adventitial layer of Control. More importantly, expression of HSP72 in media was enhanced by thermal treatment. Expression of p22-phox, the major membrane subunit of NADPH oxidase, and MCP-1 was augmented in cuff-injured adventitia of the Control but not the thermal-treated groups. Conclusions-Thermal treatment significantly attenuated infiltration of inflammatory cells in adventitia and suppressed neointimal thickening in cuff-injured arteries with the enhancement of HSP72 expression and suppression of oxidative stress.

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Section: Discussionmentioning

confidence: 86%

Thermal Treatment Attenuates Neointimal Thickening With Enhanced Expression of Heat-Shock Protein 72 and Suppression of Oxidative Stress

et al. 2004

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“…The increased intima/media ratio indicating neointimal formation, and the increased wall to lumen ratio indicating medial hyperplasia were two major hallmarks of AII induced enhancement of vascular remodeling in cuff injured artery [8] , [27] . In fact, our results also showed neointimal formation and medial hypertrophy in AII treatment ( Figure 4 ).…”

Section: Discussionmentioning

confidence: 96%

Impaired Glutathione Redox System Paradoxically Suppresses Angiotensin II-Induced Vascular Remodeling

et al. 2014

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BackgroundAngiotensin II (AII) plays a central role in vascular remodeling via oxidative stress. However, the interaction between AII and reduced glutathione (GSH) redox status in cardiovascular remodeling remains unknown.Methods In vivo: The cuff-induced vascular injury model was applied to Sprague Dawley rats. Then we administered saline or a GSH inhibitor, buthionine sulfoximine (BSO, 30 mmol/L in drinking water) for a week, subsequently administered 4 more weeks by osmotic pump with saline or AII (200 ng/kg/minute) to the rats. In vitro: Incorporation of bromodeoxyuridine (BrdU) was measured to determine DNA synthesis in cultured rat vascular smooth muscle cells (VSMCs).ResultsBSO reduced whole blood GSH levels. Systolic blood pressure was increased up to 215±4 mmHg by AII at 4 weeks (p<0.01), which was not affected by BSO. Superoxide production in vascular wall was increased by AII and BSO alone, and was markedly enhanced by AII+BSO. The left ventricular weight to body weight ratio was significantly increased in AII and AII+BSO as compared to controls (2.52±0.08, 2.50±0.09 and 2.10±0.07 mg/g respectively, p<0.05). Surprisingly, the co-treatment of BSO totally abolished these morphological changes. Although the vascular circumferential wall stress was well compensated in AII, significantly increased in AII+BSO. The anti-single-stranded DNA staining revealed increasing apoptotic cells in the neointima of injured arteries in BSO groups. BrdU incorporation in cultured VSMCs with AII was increased dose-dependently. Furthermore it was totally abolished by BSO and was reversed by GSH monoethyl ester.ConclusionsWe demonstrated that a vast oxidative stress in impaired GSH redox system totally abolished AII-induced vascular, not cardiac remodeling via enhancement of apoptosis in the neointima and suppression of cell growth in the media. The drastic suppression of remodeling may result in fragile vasculature intolerable to mechanical stress by AII.

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“…3 A-F) (9,12,(21)(22)(23). Peribronchial cuffing with implanted matrices may exacerbate injury as in other wrapped organs (24). Airflow was sufficiently restricted by combined brush denudation from within and acellular matrices from without to increase stridor Ͼ4-fold compared with injury alone.…”

Section: Discussionmentioning

confidence: 99%

Tissue-engineered endothelial and epithelial implants differentially and synergistically regulate airway repair

Zani

Kojima²,

Vacanti³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

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The trilaminate vascular architecture provides biochemical regulation and mechanical integrity. Yet regulatory control can be regained after injury without recapitulating tertiary structure. Tissue-engineered (TE) endothelium controls repair even when placed in the perivascular space of injured vessels. It remains unclear from vascular repair studies whether endothelial implants recapitulate the vascular epithelial lining or expose injured tissues to endothelial cells (ECs) with unique healing potential because ECs line the vascular epithelium and the vasa vasorum. We examined this issue in a nonvascular tubular system, asking whether airway repair is controlled by bronchial epithelial cells (EPs) or by ECs of the perfusing bronchial vasculature. Localized bronchial denuding injury damaged epithelium, narrowed bronchial lumen, and led to mesenchymal cell hyperplasia, hypervascularity, and inflammatory cell infiltration. Peribronchial TE constructs embedded with EPs or ECs limited airway injury, although optimum repair was obtained when both cells were present in TE matrices. EC and EP expression of PGE 2, TGF␤1, TGF␤2, GM-CSF, IL-8, MCP-1, and soluble VCAM-1 and ICAM-1 was altered by matrix embedding, but expression was altered most significantly when both cells were present simultaneously. EPs may provide for functional control of organ injury and fibrous response, and ECs may provide for preservation of tissue perfusion and the epithelium in particular. Together the two cells optimize functional restoration and healing, suggesting that multiple cells of a tissue contribute to the differentiated biochemical function and repair of a tissue, but need not assume a fixed, ordered architectural relationship, as in intact tissues, to achieve these effects.tissue engineering ͉ airway disease ͉ vascular disease

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Aortic Alterations in Rabbits Following Sheathing with Silastic and Polyethylene Tubes

Cited by 8 publications

References 23 publications

Thermal Treatment Attenuates Neointimal Thickening With Enhanced Expression of Heat-Shock Protein 72 and Suppression of Oxidative Stress

Thermal Treatment Attenuates Neointimal Thickening With Enhanced Expression of Heat-Shock Protein 72 and Suppression of Oxidative Stress

Impaired Glutathione Redox System Paradoxically Suppresses Angiotensin II-Induced Vascular Remodeling

Tissue-engineered endothelial and epithelial implants differentially and synergistically regulate airway repair

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