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dc.contributor.authorZand, Thomas
dc.contributor.authorNunnari, John J.
dc.contributor.authorHoffman, Allen H.
dc.contributor.authorSavilonis, Brian J.
dc.contributor.authorMacWilliams, Bruce
dc.contributor.authorMajno, G.
dc.contributor.authorJoris, Isabelle
dc.date2022-08-11T08:09:30.000
dc.date.accessioned2022-08-23T16:33:37Z
dc.date.available2022-08-23T16:33:37Z
dc.date.issued1988-11-01
dc.date.submitted2007-12-21
dc.identifier.citationAm J Pathol. 1988 Nov;133(2):407-18.
dc.identifier.issn0002-9440 (Print)
dc.identifier.pmid3189514
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38146
dc.description.abstractA 69 +/- 5% stenosis was produced in the rat aorta, with the purpose of correlating endothelial changes with local flow patterns and with levels of shear stress; the hydrodynamic data were obtained from a scaled-up model of the stenosed aorta. In the throat of the stenosis, where shear stress values were 15-25 times normal, the endothelium was stripped off within 1 hour. It regenerated at half the rate of controls but modulated into a cell type that could withstand the increased shear stress. Adaptations included changes in cell orientation, number, length, width, thickness, stress fibers, and anchoring structures, as well as changes in the length, argyrophilia, and permeability of the junctions. Areas of either elongated or "polygonal" cells consistently developed at the same sites in relation to the stenosis, but the hydrodynamic data showed that they did not always correspond (as had been anticipated) to high and low shear, respectively. It is concluded that endothelial cell shape in the living artery must be determined by some other factor(s) in addition to shear stress.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3189514&dopt=Abstract ">Link to article in PubMed</a>
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC1880795/?tool=pubmed
dc.subjectActins
dc.subject*Adaptation, Physiological
dc.subjectAnimals
dc.subjectAortic Valve Stenosis
dc.subjectEndothelium, Vascular
dc.subjectMale
dc.subjectMicroscopy, Electron
dc.subjectModels, Cardiovascular
dc.subjectRats
dc.subjectRats, Inbred Strains
dc.subjectRegional Blood Flow
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleEndothelial adaptations in aortic stenosis. Correlation with flow parameters
dc.typeJournal Article
dc.source.journaltitleThe American journal of pathology
dc.source.volume133
dc.source.issue2
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/103
dc.identifier.contextkey407398
html.description.abstract<p>A 69 +/- 5% stenosis was produced in the rat aorta, with the purpose of correlating endothelial changes with local flow patterns and with levels of shear stress; the hydrodynamic data were obtained from a scaled-up model of the stenosed aorta. In the throat of the stenosis, where shear stress values were 15-25 times normal, the endothelium was stripped off within 1 hour. It regenerated at half the rate of controls but modulated into a cell type that could withstand the increased shear stress. Adaptations included changes in cell orientation, number, length, width, thickness, stress fibers, and anchoring structures, as well as changes in the length, argyrophilia, and permeability of the junctions. Areas of either elongated or "polygonal" cells consistently developed at the same sites in relation to the stenosis, but the hydrodynamic data showed that they did not always correspond (as had been anticipated) to high and low shear, respectively. It is concluded that endothelial cell shape in the living artery must be determined by some other factor(s) in addition to shear stress.</p>
dc.identifier.submissionpathoapubs/103
dc.contributor.departmentDepartment of Pathology
dc.source.pages407-18


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