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      Rosuvastatin Suppresses the Oxidative Response in the Venous Limb of an Arteriovenous Fistula and Enhances the Fistula Blood Flow in Diabetic Rats

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          Abstract

          Objective: The blood flow in the arteriovenous (AV) fistula is significantly reduced in diabetic patients. Statins are known to mediate pleiotropic effects in the vascular endothelium and attenuate inflammatory responses. This study tested the vascular protective effect of rosuvastatin in an experimental model of AV fistula. Methods: One week after the induction of diabetes mellitus (DM) in rats, a fistula was created in the abdominal aorta and inferior vena cava. Rats received placebo or rosuvastatin (15 mg/kg/day) in chow for 2 weeks. The blood flow in the venous segments of the fistula was measured. The expression of proinflammatory genes and the generation of superoxide in the venous fistula were examined. Results: The blood flow and luminal diameter of the AV fistula was significantly enhanced in animals treated with rosuvastatin. Rosuvastatin attenuated the expression of inducible nitric oxide synthase, NADPH oxidase, and monocyte chemotactic protein-1 in the fistula. The levels of superoxide anions and proinflammatory cytokines were also suppressed in rosuvastatin-treated animals. Neointimal formation in the AV fistula was not affected following treatment with rosuvastatin. Conclusions: We demonstrated that rosuvastatin improves luminal dilatation and blood flow in the AV fistula of subjects with DM. These vascular protective effects of rosuvastatin are most likely mediated by the attenuation of proinflammatory activities in the remodeled vasculature.

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          The pleiotropic effects of statins on endothelial function, vascular inflammation, immunomodulation and thrombogenesis.

          R Shamburek, Charles A. Blum (2009)
          Statins have been demonstrated to significantly affect the prognosis and outcome of patients with risk factors to atherosclerosis (in primary and secondary prevention trials). Several clinical and recently basic studies have suggested an extra-beneficial effect of the statins in the prevention of atherosclerosis and coronary artery disease. These studies showed that statins may affect the cardiovascular system beyond their effect on the lipid profile, and it was suggested that they affect the immunological system and vascular inflammation. Many of the beneficial pleiotropic effects of statins occur as a result of modulated endothelial function and reduced inflammatory processes. Attempting to understand these properties of statins is an exciting field of research that will also improve our understanding of vascular biology in health and disease, and thus enable the better use of this drug class in clinical practice.
          Article 0 comments Cited 67 times – based on 0 reviews     Review now
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            The endothelium and vascular inflammation in diabetes.

            Martin Hartge, Ulrich Kintscher, THOMAS UNGER (2007)
            The endothelium releases multiple mediators, not only regulators of vasomotor function but also important physiological and pathophysiological inflammatory mediators. Endothelial dysfunction is caused by chronic exposure to various stressors such as oxidative stress and modified low-density lipoprotein (LDL) cholesterol, resulting in impaired nitric oxide (NO) production and chronic inflammation. Biomechanical forces on the endothelium, including low shear stress from disturbed blood flow and hypertension, are also important causes of endothelial dysfunction. These processes seem to be augmented in patients with diabetes. In states of insulin resistance and in type 2 diabetes insulin signalling is impaired. Increased vascular inflammation, including enhanced expression of interleukin- 6 (IL-6), vascular cellular adhesion molecule-1 (VCAM-1) and monocyte chemoattractant protein (MCP- 1) are observed, as is a marked decrease in NO bioavailability. Furthermore, hyperglycaemia leads to increased formation of advanced glycation end products (AGE), which quench NO and impair endothelial function. In summary, during the development of diabetes a number of biochemical and mechanical factors converge on the endothelium, resulting in endothelial dysfunction and vascular inflammation. In the presence of insulin resistance, these processes are potentiated and they provide a basis for the macrovascular disease seen in diabetes.
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              Early arteriovenous fistula failure: a logical proposal for when and how to intervene.

              Prabir Roy-Chaudhury, Arif Asif, Gerald A Beathard (2006)
              A significant number of arteriovenous fistulae (28 to 53%) never mature to support dialysis. Often, renal physicians and surgeons wait for up to 6 months and even longer hoping that the arteriovenous fistula (AVF) will eventually grow to support dialysis before declaring that the AVF has failed. In the interim, if dialysis is needed, then a tunneled catheter is inserted, exposing the patient to the morbidity and mortality associated with the use of this device. In general, a blood flow of 500 ml/min and a diameter of at least 4 mm are needed for an AVF to be adequate to support dialysis therapy. In most successful fistulae, these parameters are met within 4 to 6 wk. Most important, commonly encountered problems (stenosis and accessory veins) that result in early AVF failure can be diagnosed easily with skillful physical examination. Recent studies have indicated that a great majority of fistulae that have failed to mature adequately can be salvaged by percutaneous interventions and become available for dialysis. Early intervention regarding identification and salvage of a nonmaturing AVF is critical for several reasons. First, an AVF is the best available type of access regarding complications, costs, morbidity, and mortality. Second, this approach minimizes catheter use and its associated complications. Finally, access stenosis is a progressive process and eventually culminates in complete occlusion, leading to access thrombosis. In this context, the opportunity to salvage the AVF that fails early may be lost. This report reviews the process of AVF maturation and suggests a strategy for when and how to intervene to identify and salvage AVF with early failure.
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                Author and article information

                Journal
                Journal ID (publisher-id): JVR
                Journal ID (nlm-ta): J Vasc Res
                Journal ID (doi): 10.1159/issn.1018-1172
                Title: Journal of Vascular Research
                Publisher: S. Karger AG
                ISSN (Print): 1018-1172
                ISSN (Electronic): 1423-0135
                Publication date Subscription-year: 2014
                Publication date (Print): June 2014
                Publication date (Electronic): 15 January 2014
                Volume: 51
                Issue: 2
                Pages: 81-89
                Affiliations
                aDepartments of Anesthesiology and bInternal Medicine, cInstitute of Clinical Medicine, and dDivision of Cardiovascular Surgery, Department of Surgery, National Cheng Kung University Hospital and College of Medicine, National Cheng Kung University, and eDepartment of Biotechnology, Chia Nan University of Pharmacy and Science, Tainan, and fDepartment of Anesthesiology, Buddhist Tzu-Chi General Hospital and Tzu-Chi University School of Medicine, Hualien, Taiwan
                Author notes
                *Dr. Chen-Fuh Lam, Department of Anesthesiology, Buddhist Tzu-Chi General Hospital and Tzu-Chi University School of Medicine, 707 Chung-Yang Road, 970 Hualien (Taiwan), E-Mail lamcf@mail.ncku.edu.tw, lamcf@tzuchi.com.tw
                Article
                Publisher ID: 357619 Other ID: J Vasc Res 2014;51:81-89
                DOI: 10.1159/000357619
                PubMed ID: 24434545
                SO-VID: 8f4c39f5-d7d7-4c67-84ff-0db6abb374f9
                Copyright © © 2014 S. Karger AG, Basel
                License:

                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.

                History
                Date received : 25 February 2013
                Date accepted : 24 November 2013
                Page count
                Figures: 5, Tables: 2, Pages: 9
                Categories
                Subject: Research Paper

                ScienceOpen disciplines: General medicine,Neurology,Cardiovascular Medicine,Internal medicine,Nephrology
                Keywords: Superoxide,Intimal hyperplasia,Hemodialysis,Arteriovenous shunt,Peripheral vascular diseases,Inflammation,HMG-CoA reductase inhibitors
                Data availability:
                ScienceOpen disciplines: General medicine, Neurology, Cardiovascular Medicine, Internal medicine, Nephrology
                Keywords: Superoxide, Intimal hyperplasia, Hemodialysis, Arteriovenous shunt, Peripheral vascular diseases, Inflammation, HMG-CoA reductase inhibitors

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