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      External Collar Inhibits Balloon-Induced Intimal Hyperplasia in Rabbits

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      Journal of Vascular Research

      S. Karger AG

      Adventitia, Intimal hyperplasia, Angioplasty, Collar

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          Abstract

          Intimal hyperplasia is a common complication following vascular interventions. To understand the underlying pathophysiology, the focus has mainly been on the intima and media. The adventitia has been less investigated, although adventitial hyperplasia is seen together with intimal hyperplasia. If the adventitial response is an important part of the process, the adventitia might be a target to inhibit intimal hyperplasia. In the present study we investigated whether an external collar attenuating the adventitial thickness could inhibit a balloon-induced intimal hyperplasia. The common carotid artery was injured in rabbits (n = 6) with a 3-french balloon catheter. The mid portion of the injured artery was encircled with a silicone collar (diameter = 2.0 mm). After 14 days the balloon-induced neointima was reduced by 54 ± 6.3% underneath the collar. The adventitial and medial thickenings were also attenuated (36 ± 8.7 and 44 ± 4.3%, respectively). This study demonstrates that intimal hyperplasia following balloon injury can be inhibited with an external collar. This supports the idea of the adventitia as a potential target to inhibit intimal hyperplasia.

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          Most cited references 5

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          Neuropeptide Y stimulates proliferation of human vascular smooth muscle cells: cooperation with noradrenaline and ATP.

          Since the sympathetic nervous system has been shown to exert a trophic influence on vascular smooth muscle cells (SMC), we studied the growth regulating effects of neuropeptide Y (NPY) in cooperation with the sympathetic co-transmitters noradrenaline and adenosine triphosphate (ATP) in human vascular SMC. NPY stimulated DNA synthesis in human SMC grown from subcutaneous arteries and veins (diameter: 0.4 mm) measured by [3H]thymidine incorporation. Also cell number and protein synthesis were stimulated. The effect was mediated through the Y1-receptor and not Y2 or Y3 since the Y1-selective NPY analogue Pro34-NPY and peptide YY stimulated mitogenesis in the same magnitude as NPY while the NPY-fragment NPY13-36 only had minor effects. The effect was blocked by pretreating the cells with pertussis toxin indicating a Gi/o-coupled effect. The other sympathetic co-transmitters, noradrenaline and ATP, also stimulated mitogenesis in the human SMC in a similar magnitude as NPY. When added together NPY and noradrenaline potentiated each other in the mitogenic response. ATP had mainly additive effects. This is the first demonstration that NPY, noradrenaline and ATP stimulates growth in human vascular SMC. This suggests a role of the sympathetic cotransmitters in modulating vascular tone, but also by inducing hypertrophy/hyperplasia with possible clinical consequences.
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            Macro-porosity is necessary for the reduction of neointimal and medial thickening by external stenting of porcine saphenous vein bypass grafts.

            placing external non-restrictive macro-porous stents around porcine vein grafts prevents neointima formation and medial thickening in both the short and long term. Whether the porosity of the stent material influences this effect, however, has not been determined. Therefore, the effect on neointimal and medial thickening of external macro-porous (polyester) and micro-porous (polytetrafluorethylene) stents of equal diameter were compared. The effect on expression of platelet-derived growth factor (PDGF), a potent mediator of vascular smooth muscle cell migration and proliferation and its receptors was also investigated. saphenous vein-carotid artery interposition grafting was performed in Landrace pigs with external placement of 8 mm diameter macro- and micro-porous stents contralaterally. One month after surgery, graft wall dimensions, PDGF and PDGF receptor expression and cell proliferation using proliferating cell nuclear antigen (PCNA) were measured on histological sections. Macro-porous stents significantly reduced neointimal and medial thickening compared with micro-porous stents (0.1+/-0.02 vs. 0.25+/-0.03 mm, P<0.002, and 0.10+/-0.02 vs. 0.17+/-0.02 mm, P<0.014, respectively). Macro-porous stents significantly reduced the percentage of cells expressing PDGF and PCNA, compared with micro-porous stents (36+/-9 vs. 80+/-7, P < 0.002, and 11+/-3 vs. 21+/-2, P < 0.02, respectively). The percentage of cells expressing PDGF receptors was similar with both the stent types. Adventitial microvessel formation occurred across macro-porous stents but was markedly suppressed by micro-porous stents. porosity is crucial to the efficacy of external stents in reducing neointima formation in porcine vein grafts. Decreases in PDGF expression and cell proliferation accompany the reduction in neointima formation. In addition, macro-porous stents allow adventitial microvessels to connect with the vasculature outside the stent, thereby potentially improving oxygenation. Although external stenting is highly effective in reducing neointima formation after vein grafting, the properties of the stent material necessary for this effect have not been defined. This study establishes that macro-porosity is one essential feature required to reduce PDGF expression cell proliferation and neointima formation.
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              Mitogenic effect of neuropeptide Y in rat vascular smooth muscle cells

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                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
                2002
                August 2002
                12 August 2002
                : 39
                : 4
                : 361-367
                Affiliations
                Wallenberg Laboratory for Cardiovascular Research, Department of Vascular Surgery, Sahlgrenska University Hospital, Göteborg, Sweden
                Article
                65548 J Vasc Res 2002;39:361–367
                10.1159/000065548
                12187126
                © 2002 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: 6, Tables: 2, References: 32, Pages: 7
                Categories
                Research Paper

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