0
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found

      Intimal Hyperplasia in Mouse Vein Grafts Is Regulated by Flow

      ,

      Journal of Vascular Research

      S. Karger AG

      Shear stress, Flow, Intimal hyperplasia, Mice, Vein graft

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Altered flow conditions are presumed to cause stenosis in vein grafts due to exaggerated neointimal formation. The aim of this study was to establish a mouse model of flow-regulated intimal hyperplasia (IH) in vein grafts. The caval vein was grafted into the common carotid artery of 38 mice, followed by modulation of the blood flow, resulting in vein grafts with high (HF) and low flow (LF). The vessel wall thickening was evaluated after 3, 14 and 42 days by morphometric analyses and immunohistochemistry. There was an immediate significant change in flow, which was persistent throughout the time of observation. After 42 days, flow was increased 2.7 times in HF animals compared to LF animals. The vessel wall was composed of two layers where the inner layer was positive for α-actin and considered as IH. The area of neointimal formation was 74% larger in the LF group compared to the HF group. The present study demonstrates that flow regulates IH in vein grafts in mice. This model gives the potential to study the effect of shear stress on vascular biology in genetically modified animals.

          Related collections

          Most cited references 17

          • Record: found
          • Abstract: found
          • Article: not found

          Direct evidence for the importance of endothelium-derived nitric oxide in vascular remodeling.

          The vascular endothelium mediates the ability of blood vessels to alter their architecture in response to hemodynamic changes; however, the specific endothelial-derived factors that are responsible for vascular remodeling are poorly understood. Here we show that endothelial-derived nitric oxide (NO) is a major endothelial-derived mediator controlling vascular remodeling. In response to external carotid artery ligation, mice with targeted disruption of the endothelial nitric oxide synthase gene (eNOS) did not remodel their ipsilateral common carotid arteries whereas wild-type mice did. Rather, the eNOS mutant mice displayed a paradoxical increase in wall thickness accompanied by a hyperplastic response of the arterial wall. These findings demonstrate a critical role for endogenous NO as a negative regulator of vascular smooth muscle proliferation in response to a remodeling stimulus. Furthermore, our data suggests that a primary defect in the NOS/NO pathway can promote abnormal remodeling and may facilitate pathological changes in vessel wall morphology associated with complex diseases such as hypertension and atherosclerosis.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Diverse contribution of bone marrow cells to neointimal hyperplasia after mechanical vascular injuries.

            We and others have suggested that bone marrow-derived progenitor cells may contribute to the pathogenesis of vascular diseases. On the other hand, it was reported that bone marrow cells do not participate substantially in vascular remodeling in other experimental systems. In this study, three distinct types of mechanical vascular injuries were induced in the same mouse whose bone marrow had been reconstituted with that of GFP or LacZ mice. All injuries are known to cause smooth muscle cell (SMC) hyperplasia. At 4 weeks after wire-mediated endovascular injury, a significant number of the neointimal and medial cells derived from bone marrow. In contrast, marker-positive cells were seldom detected in the lesion induced by perivascular cuff replacement. There were only a few bone marrow-derived cells in the neointima after ligation of the common carotid artery. These results indicate that the origin of intimal cells is diverse and that contribution of bone marrow-derived cells to neointimal hyperplasia depends on the type of model.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Anastomotic intimal hyperplasia: mechanical injury or flow induced.

              All anastomotic intimal thickening may not be the same, and the underlying mechanism(s) regulating the different types may vary. We investigated the localization of experimental anastomotic intimal thickening in relation to known biomechanical and hemodynamic factors. Bilateral iliofemoral saphenous vein and polytetrafluoroethylene grafts were implanted in 13 mongrel dogs. The distal end-to-side anastomotic geometry was standardized, and the flow parameters were measured. After 8 weeks, seven of 10 animals (group I) with patent grafts were killed and the anastomoses fixed by perfusion. Histologic sections from each anastomosis were studied with light microscopy, and regions of intimal thickening were identified and quantitated with use of oculomicrometry. To characterize the anastomotic flow patterns, transparent silicone models were constructed from castings of the distal anastomosis of three animals (group II), and flow was visualized with use of helium-neon laser-illuminated particles under conditions simulating the in vivo pulsatile flow parameters. Histologic sections revealed two separate and distinct regions of anastomotic intimal thickening. The first, suture line intimal thickening, was greater in polytetrafluoroethylene anastomoses (0.35 +/- 0.23 microns) than in vein anastomoses (0.15 +/- 0.03 microns, p less than 0.05). The second distinct type of intimal thickening developed on the arterial floor and was the same in polytetrafluoroethylene (0.11 +/- 0.11 microns) and vein anastomoses (0.12 +/- 0.03 microns). Model flow visualization studies revealed a flow stagnation point along the arterial floor resulting in a region of low and oscillating shear where the second type of intimal thickening developed. High shear and short particle residence time were observed along the hood of the graft, an area devoid of intimal thickening.(ABSTRACT TRUNCATED AT 250 WORDS)
                Bookmark

                Author and article information

                Journal
                JVR
                J Vasc Res
                10.1159/issn.1018-1172
                Journal of Vascular Research
                S. Karger AG
                1018-1172
                1423-0135
                2005
                February 2005
                28 January 2005
                : 42
                : 1
                : 13-20
                Affiliations
                Wallenberg Laboratory for Cardiovascular Research and Department of Vascular Surgery, Sahlgrenska Academy, Göteborg University, Göteborg, Sweden
                Article
                82802 J Vasc Res 2005;42:13–20
                10.1159/000082802
                15608438
                © 2005 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 4, Tables: 1, References: 28, Pages: 8
                Categories
                Research Paper

                Comments

                Comment on this article