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      Effects of Nicotine on Angiogenesis and Restenosis in a Rabbit Model

      , , ,

      Cardiology

      S. Karger AG

      Restenosis, Nicotine, Angiogenesis, Rabbit

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          Abstract

          Background and Aims: Nicotine is a major component of cigarette smoke and has been found to play an important role in angiogenesis. However, whether nicotine plays a role in restenosis has not been determined. Therefore, the aim of the present study was to determine the effects of nicotine on angiogenesis and restenosis in a rabbit model. Methods: Forty male New Zealand White rabbits were randomly divided into control and low-, middle-, and high-dose (0.005, 0.05 or 5 µg/kg, respectively) nicotine-treated groups. Balloon catheter denuding injury iliac artery and ligation of left anterior descending coronary artery were performed in all animals fed with a high-cholesterol diet (HCD) beginning 2 weeks before operation. Nicotine was administered daily by intramuscular injection in the ischemic hindlimb for 3 weeks. Control rabbits received an equal volume of phosphate-buffered saline alone. Collateral vessels of the ischemic hindlimb were observed by angiography of abdominal aorta, and the density of intramyocardial microvessels and proliferative activity of balloon-injured arteries were examined by immunohistochemistry. Serum levels of lipids and the indexes of hepatic or renal functions were also determined before HCD and after nicotine treatment. Results: One rabbit in control, two in low-, one in middle- and two in high-dose groups died during the experiment. The remaining 34 rabbits were included in the study. Two or five weeks after HCD, the levels of serum lipids were significantly increased in all groups, but there was no significant difference of the levels between control and nicotine-treated groups 3 weeks after treatment; the indexes of hepatic or renal functions showed no significant changes 3 weeks after nicotine treatment; there were no significant differences on collateral vessels shown by angiography in all four groups; the density of intramyocardial microvessels in three nicotine-treated groups was significantly higher than that in control group; but the intimal area and proliferative activity in the balloon-injured arteries in three nicotine-treated groups were also higher than those in control group. Conclusions: The present study shows that intramuscular administration of nicotine for 3 weeks could not increase arteriogenesis in ischemic hindlimb of rabbits, but is capable of significantly promoting intramyocardial angiogenesis. Nicotine can also accelerate intimal proliferation and thickening of balloon catheter denuding injury iliac artery, so it may contribute to the development of restenosis.

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          Most cited references 20

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          Nicotine stimulates angiogenesis and promotes tumor growth and atherosclerosis.

          We provide anatomic and functional evidence that nicotine induces angiogenesis. We also show that nicotine accelerates the growth of tumor and atheroma in association with increased neovascularization. Nicotine increased endothelial-cell growth and tube formation in vitro, and accelerated fibrovascular growth in vivo. In a mouse model of hind-limb ischemia, nicotine increased capillary and collateral growth, and enhanced tissue perfusion. In mouse models of lung cancer and atherosclerosis, we found that nicotine enhanced lesion growth in association with an increase in lesion vascularity. These effects of nicotine were mediated through nicotinic acetylcholine receptors at nicotine concentrations that are pathophysiologically relevant. The endothelial production of nitric oxide, prostacyclin and vascular endothelial growth factor might have a role in these effects.
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            Monocyte activation in angiogenesis and collateral growth in the rabbit hindlimb.

            We have previously shown that monocytes adhere to the vascular wall during collateral vessel growth (arteriogenesis) and capillary sprouting (angiogenesis). In this study we investigated the association of monocyte accumulation with both the production of the cytokines-basic fibroblast growth factor (bFGF) and TNF-alpha-and vessel proliferation in the rabbit after femoral artery occlusion. In particular, we studied the effects of an increase in monocyte recruitment by LPS on capillary density as well as collateral and peripheral conductance after 7 d of occlusion. Monocytes accumulated around day 3 in collateral arteries when maximal proliferation was observed, and stained strongly for bFGF and TNF-alpha. In the lower limb where angiogenesis was shown to be predominant, macrophage accumulation was also closely associated with maximal proliferation (around day 7). LPS treatment significantly increased capillary density (424+/-26.1 n/mm2 vs. 312+/-20.7 n/mm2; P < 0.05) and peripheral conductance (109+/-33.8 ml/min/100 mmHg vs. 45+/-6.8 ml/min/100 mmHg; P < 0.05) as compared with untreated animals after 7 d of occlusion. These results indicate that monocyte activation plays a major role in angiogenesis and collateral artery growth.
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              Transdermal nicotine for active ulcerative colitis.

              Ulcerative colitis is largely a disease of nonsmokers. Because anecdotal reports suggest that smoking and nicotine may improve the symptoms of the disease, we examined the effect of nicotine as a supplemental treatment for ulcerative colitis. We treated 72 patients with active ulcerative colitis with either transdermal nicotine patches or placebo patches for six weeks in a randomized, double-blind study. Incremental doses of nicotine were given; most patients tolerated doses of 15 to 25 mg per 24 hours. All the patients had been taking mesalamine, and 12 were receiving low doses of glucocorticoids; these medications were continued without change during the study. Clinical, sigmoidoscopic, and histologic assessments were made at base line and at the end of the study; symptoms were recorded daily on a diary card, and the clinician made a global assessment. Side effects and plasma nicotine and cotinine concentrations were monitored throughout the study. Seventeen of the 35 patients in the nicotine group had complete remissions, as compared with 9 of the 37 patients in the placebo group (P = 0.03). The patients in the nicotine group had greater improvement in the global clinical grade of colitis (P < 0.001) and the histologic grade (P = 0.03), lower stool frequency (a difference of 1.6 stools daily; P = 0.008), less abdominal pain (P = 0.05), and less fecal urgency (P = 0.009). More patients in the nicotine group had side effects (23, vs. 11 in the placebo group; P = 0.002), the most common of which were nausea, lightheadedness, headache, and sleep disturbance. Withdrawals due to ineffective therapy were more common in the placebo group (3 vs. 8, P = 0.12). The addition of transdermal nicotine to conventional maintenance therapy improves symptoms in patients with ulcerative colitis.
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                Author and article information

                Journal
                CRD
                Cardiology
                10.1159/issn.0008-6312
                Cardiology
                S. Karger AG
                0008-6312
                1421-9751
                2007
                February 2007
                21 July 2006
                : 107
                : 2
                : 122-131
                Affiliations
                Department of Cardiology, Institute of Cardiovascular Diseases, the First Affiliated Hospital, Guangxi Medical University, Guangxi, China (PR)
                Article
                94658 Cardiology 2007;107:122–131
                10.1159/000094658
                16864991
                © 2007 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: 3, References: 31, Pages: 10
                Categories
                Original Research

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