Resistance Artery Mechanics, Structure, and Extracellular Components in Spontaneously Hypertensive Rats

Intengan, Hope D.; Thibault, Gaétan; Li, Jinsheng; Schiffrin, Ernesto L.

doi:10.1161/01.cir.100.22.2267

Cited by 195 publications

(156 citation statements)

References 30 publications

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“…Despite the samples being incubated for 20 hours, thicker samples will require longer for the enzymes to permeate to the centre and thus thinner samples would be expected to be more digested [48].…”

Section: Mechanical Tests and Effects Of Digestionmentioning

confidence: 99%

Creating a model of diseased artery damage and failure from healthy porcine aorta

Noble

Smulders

Green

et al. 2016

Journal of the Mechanical Behavior of Biomedical Materials

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Article available under the terms of the CC-BY-NC-ND licence (https://creativecommons.org/licenses/by-nc-nd/4.0/) eprints@whiterose.ac.uk https://eprints.whiterose.ac.uk/ Reuse Unless indicated otherwise, fulltext items are protected by copyright with all rights reserved. The copyright exception in section 29 of the Copyright, Designs and Patents Act 1988 allows the making of a single copy solely for the purpose of non-commercial research or private study within the limits of fair dealing. The publisher or other rights-holder may allow further reproduction and re-use of this version -refer to the White Rose Research Online record for this item. Where records identify the publisher as the copyright holder, users can verify any specific terms of use on the publisher's website. TakedownIf you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing eprints@whiterose.ac.uk including the URL of the record and the reason for the withdrawal request.Creating a model of diseased artery damage and failure from healthy porcine aorta AbstractLarge quantities of diseased tissue are required in the research and development of new generations of medical devices, for example for use in physical testing. However, these are difficult to obtain. In contrast, porcine arteries are readily available as they are regarded as waste. Therefore, reliable means of creating from porcine tissue physical models of diseased human tissue that emulate well the associated mechanical changes would be valuable. To this end, we studied the effect on mechanical response of treating porcine thoracic aorta with collagenase, elastase and glutaraldehyde. The alterations in mechanical and failure properties were assessed via uniaxial tension testing. A constitutive model composed of the Gasser-Ogden-Holzapfel model, for elastic response, and a continuum damage model, for the failure, was also employed to provide a further basis for comparison [1,2]. For the concentrations used here it was found that: collagenase treated samples showed decreased fracture stress in the axial direction only; elastase treated samples showed increased fracture stress in the circumferential direction only; and glutaraldehyde samples showed no change in either direction. With respect to the proposed constitutive model, both collagenase and elastase had a strong effect on the fibre-related terms. The model more closely captured the tissue response in the circumferential direction, due to the smoother and sharper transition from damage initiation to complete failure in this direction. Finally, comparison of the results with those of tensile tests on diseased tissues suggests these treatments indeed provide a basis for creation of physical models of diseased arteries.

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Section: Mechanical Tests and Effects Of Digestionmentioning

confidence: 99%

Creating a model of diseased artery damage and failure from healthy porcine aorta

Noble

Smulders

Green

et al. 2016

Journal of the Mechanical Behavior of Biomedical Materials

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show abstract

“…The collagen/ elastin ratio has also been shown to be increased in human resistance arteries from mild essential hypertensive patients. [55][56][57] Moreover, vascular proteoglycan synthesis is also increased by high blood pressure. 58 These changes may contribute to the inward remodeling of the arterioles found in hypertension.…”

Section: Composition Of the Extracellular Matrix (Ecm) In The Vasculamentioning

confidence: 99%

Prevention and regression of hypertension: role of renal microvascular protection

et al. 2009

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Hypertension is a disease which affects over 26.4% of the world adult population, therefore novel approaches to the prevention and treatment of this disease need to be examined. Previous studies from our and other laboratories have shown that treatment of spontaneously hypertensive rats (SHR) and Dahl salt-sensitive rats with a renin-angiotensin system (RAS) inhibitor during the 'critical period' in hypertension development results in prevention of the later development of hypertension. In humans, Julius et al. reported similar findings in the landmark TROPHY study. Recently, we reported that 'pulse' treatment of SHR with highdose angiotensin receptor blocker (ARB) is effective in causing sustained reduction of already established hypertension, even when the treatment was started after the 'critical period'. These results suggest the possibility that 'regression' of established hypertension may become feasible, and we have started a prospective, multicenter clinical study (STAR CAST study) to examine this possibility. In our animal studies, we found that treatment of rats during the 'critical period' with an ARB inhibits the development of renal arteriolar hypertrophy. Moreover, a high-dose angiotensin blocker caused a remarkable reversal of renal arteriolar hypertrophy in SHR, which was associated with changes in microvascular MMP expression. These results suggest that changes in the renal microvasculature may have an important role in the mechanisms of hypertension prevention and regression by ARB.

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“…Previous studies have shown that av integrin levels are enhanced on the dysfunctional endothelium in spontaneously hypertensive rats, but not in controls. 25 This therefore allowed the evaluation of FLT-1 activity and RGD targeting with a single vector system in a disease model. We used short exposure times of virus:vessel (30 and 60 min), since this is a limitation for vascular gene delivery.…”

mentioning

confidence: 99%

Dual targeting of gene delivery by genetic modification of adenovirus serotype 5 fibers and cell-selective transcriptional control

et al. 2004

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Adenovirus (Ad)-mediated gene delivery is a promising approach for genetic manipulation of the vasculature and is being used in both preclinical models and clinical trials. However, safety concerns relating to infection of nontarget tissue and the poor infectivity of vascular cells compared to other cell types necessitates Ad vector refinement. Here, we combine a transductional targeting approach to improve vascular cell infectivity through RGD peptide insertion into adenovirus fibers, combined with transcriptional targeting to endothelial cells using a E1 kb fragment of the fms-like tyrosine kinase receptor-1 (FLT-1) promoter. Single-and double-modified vectors were characterized in human cell lines that either support or have silenced FLT-1 expression.In rat hepatocytes and endothelial cells, the double modification substantially shifted transduction profiles toward vascular endothelial cells. Furthermore, in intact aortae derived from spontaneously hypertensive rats that display enhanced av integrin expression on dysfunctional endothelium, enhanced levels of transduction were observed using the double-modified vector but not in aortae derived from normotensive control rats. Our data indicate that Admediated transduction can be beneficially modified in vitro and in vivo by combining fiber modification and a cellselective promoter within a single-component vector system.

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Resistance Artery Mechanics, Structure, and Extracellular Components in Spontaneously Hypertensive Rats

Cited by 195 publications

References 30 publications

Creating a model of diseased artery damage and failure from healthy porcine aorta

Creating a model of diseased artery damage and failure from healthy porcine aorta

Prevention and regression of hypertension: role of renal microvascular protection

Dual targeting of gene delivery by genetic modification of adenovirus serotype 5 fibers and cell-selective transcriptional control

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