J M Bellón, F Jurado, M P De Miguel, B Fraile, J Buján
{"title":"Long-term behavior of an arterial autograft: a new role for intimal hyperplasia?","authors":"J M Bellón, F Jurado, M P De Miguel, B Fraile, J Buján","doi":"10.1159/000179180","DOIUrl":null,"url":null,"abstract":"<p><p>The long-term behavior of an arterial autograft was studied with special attention to the evolution of intimal hyperplasia. An arterial autograft measuring approximately 5 mm in length was implanted in the right common iliac artery of female Sprague-Dawley rats. Animals were sacrificed at 90, 120, 150, 180, 240, 360, 400, 540 and 730 days after implantation. Grafts were evaluated by optical microscopy, electron microscopy, and morphometry. Myointimal cells were marked using an antiactin monoclonal antibody and studied by transmission electron microscopy. In the long term, the myointima of the arterial wall appeared as a consolidated layer formed by smooth muscle cells of contractile phenotype, abundant extracellular material consisting of clumps of elastin and collagen fibers. Cell maturity and degree of differentiation were demonstrated by the incorporation of antiactin antibody. The medial layer of the grafted segment suffered a marked long-term loss of cells and became an acellular layer sustained by the elastic layers. The adventitial layer was markedly cellular and had abundant vasa vasorum. Morphometry showed that the myointimal layer in the operated territory was not uniform and consisted of tongues of varying thickness. The total thickness of the arterial wall did not differ significantly (p > 0.05) between the graft and the proximal and distal areas. The results suggest that the intimal hyperplasia originating during the repair process could assume some functions of the degenerated medial layer, maintaining long-term vascular homeostasis.</p>","PeriodicalId":14035,"journal":{"name":"International journal of microcirculation, clinical and experimental","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1996-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000179180","citationCount":"7","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International journal of microcirculation, clinical and experimental","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000179180","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 7
Abstract
The long-term behavior of an arterial autograft was studied with special attention to the evolution of intimal hyperplasia. An arterial autograft measuring approximately 5 mm in length was implanted in the right common iliac artery of female Sprague-Dawley rats. Animals were sacrificed at 90, 120, 150, 180, 240, 360, 400, 540 and 730 days after implantation. Grafts were evaluated by optical microscopy, electron microscopy, and morphometry. Myointimal cells were marked using an antiactin monoclonal antibody and studied by transmission electron microscopy. In the long term, the myointima of the arterial wall appeared as a consolidated layer formed by smooth muscle cells of contractile phenotype, abundant extracellular material consisting of clumps of elastin and collagen fibers. Cell maturity and degree of differentiation were demonstrated by the incorporation of antiactin antibody. The medial layer of the grafted segment suffered a marked long-term loss of cells and became an acellular layer sustained by the elastic layers. The adventitial layer was markedly cellular and had abundant vasa vasorum. Morphometry showed that the myointimal layer in the operated territory was not uniform and consisted of tongues of varying thickness. The total thickness of the arterial wall did not differ significantly (p > 0.05) between the graft and the proximal and distal areas. The results suggest that the intimal hyperplasia originating during the repair process could assume some functions of the degenerated medial layer, maintaining long-term vascular homeostasis.