Effects of an Inhibitor of Nitric Oxide Synthesis on Skin Wound Repair
Identifieur interne : 004142 ( Istex/Corpus ); précédent : 004141; suivant : 004143Effects of an Inhibitor of Nitric Oxide Synthesis on Skin Wound Repair
Auteurs : Tp Amadeu ; A. Desmoulière ; Ama CostaSource :
- Wound Repair and Regeneration [ 1067-1927 ] ; 2005-01.
Abstract
Considering that nitric oxide (NO) plays an important role on cutaneous wound repair, but its effects have not been defined, an inhibitor of NO synthesis (LNAME) was used. Control group received free water and LNAME group received LNAME (20 mg/kg/day) in drinking water. A full‐thickness excisional wound was performed (0d), and the animals were sacrificed 7, 14, and 21 days later. Wound contraction was evaluated by lesion surface measurement at 0d, 7d, 14d, and 21d. The blood pressure of all rats was measured in the beginning and at the each time point of the experiment with a plethysmography method. The wound and normal skin surrounding was formol fixed and paraffin embedded. To evaluate the vessels, an immunohistochemistry for α‐smooth muscle actin was done and stereological parameters were estimated in superficial and deep dermis. At 7d, 14d, and 21d the blood pressure of LNAME group was higher compared with control group (p < 0.001 for all). The wound contraction of LNAME group was slower compared with control group at 14d and 21d (p = 0.004 for both). In superficial dermis, vessels were more dilated in control group compared with LNAME group at 14d and 21d (p = 0.02; p < 0.0001, respectively) and longer in control group compared with LNAME group at 7d and 14d (p = 0.043; p = 0.002, respectively). Deep dermal vessels were more prominent and dilated in control group compared with LNAME group at 21d (p = 0.003; p = 0.0007, respectively), but at 7d, vessels were more dilated in LNAME group compared with control group (p = 0.015). In deep dermis, vessels were longer in control group compared with LNAME group at 14d and 21d (p = 0.002; p = 0.046, respectively). Our results show that nitric oxide inhibition affects the wound contraction and the vascularization pattern, mainly in the later phases of skin wound repair.
Url:
DOI: 10.1111/j.1067-1927.2005.130117f.x
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Effects of an Inhibitor of Nitric Oxide Synthesis on Skin Wound Repair</title><author><name sortKey="Amadeu, Tp" sort="Amadeu, Tp" uniqKey="Amadeu T" first="Tp" last="Amadeu">Tp Amadeu</name><affiliation><mods:affiliation>Histology and Embryology Department, State University of Rio de Janeiro, RJ, Brazil,</mods:affiliation></affiliation></author><author><name sortKey="Desmouliere, A" sort="Desmouliere, A" uniqKey="Desmouliere A" first="A" last="Desmoulière">A. Desmoulière</name><affiliation><mods:affiliation>INSERM E0362, Université Victor Segalen, Bordeaux, France</mods:affiliation></affiliation></author><author><name sortKey="Costa, Ama" sort="Costa, Ama" uniqKey="Costa A" first="Ama" last="Costa">Ama Costa</name><affiliation><mods:affiliation>Histology and Embryology Department, State University of Rio de Janeiro, RJ, Brazil,</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:8AF75EE739A6543EB8CE5D86B4834D4EF3213319</idno><date when="2005" year="2005">2005</date><idno type="doi">10.1111/j.1067-1927.2005.130117f.x</idno><idno type="url">https://api.istex.fr/document/8AF75EE739A6543EB8CE5D86B4834D4EF3213319/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">004142</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">004142</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">Effects of an Inhibitor of Nitric Oxide Synthesis on Skin Wound Repair</title><author><name sortKey="Amadeu, Tp" sort="Amadeu, Tp" uniqKey="Amadeu T" first="Tp" last="Amadeu">Tp Amadeu</name><affiliation><mods:affiliation>Histology and Embryology Department, State University of Rio de Janeiro, RJ, Brazil,</mods:affiliation></affiliation></author><author><name sortKey="Desmouliere, A" sort="Desmouliere, A" uniqKey="Desmouliere A" first="A" last="Desmoulière">A. 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Control group received free water and LNAME group received LNAME (20 mg/kg/day) in drinking water. A full‐thickness excisional wound was performed (0d), and the animals were sacrificed 7, 14, and 21 days later. Wound contraction was evaluated by lesion surface measurement at 0d, 7d, 14d, and 21d. The blood pressure of all rats was measured in the beginning and at the each time point of the experiment with a plethysmography method. The wound and normal skin surrounding was formol fixed and paraffin embedded. To evaluate the vessels, an immunohistochemistry for α‐smooth muscle actin was done and stereological parameters were estimated in superficial and deep dermis. At 7d, 14d, and 21d the blood pressure of LNAME group was higher compared with control group (p < 0.001 for all). The wound contraction of LNAME group was slower compared with control group at 14d and 21d (p = 0.004 for both). In superficial dermis, vessels were more dilated in control group compared with LNAME group at 14d and 21d (p = 0.02; p < 0.0001, respectively) and longer in control group compared with LNAME group at 7d and 14d (p = 0.043; p = 0.002, respectively). Deep dermal vessels were more prominent and dilated in control group compared with LNAME group at 21d (p = 0.003; p = 0.0007, respectively), but at 7d, vessels were more dilated in LNAME group compared with control group (p = 0.015). In deep dermis, vessels were longer in control group compared with LNAME group at 14d and 21d (p = 0.002; p = 0.046, respectively). 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Amadeu</name><affiliations><json:string>Histology and Embryology Department, State University of Rio de Janeiro, RJ, Brazil,</json:string></affiliations></json:item><json:item><name>A Desmoulière</name><affiliations><json:string>INSERM E0362, Université Victor Segalen, Bordeaux, France</json:string></affiliations></json:item><json:item><name>AMA Costa</name><affiliations><json:string>Histology and Embryology Department, State University of Rio de Janeiro, RJ, Brazil,</json:string></affiliations></json:item></author><articleId><json:string>WRR130117F</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>abstract</json:string></originalGenre><abstract>Considering that nitric oxide (NO) plays an important role on cutaneous wound repair, but its effects have not been defined, an inhibitor of NO synthesis (LNAME) was used. Control group received free water and LNAME group received LNAME (20 mg/kg/day) in drinking water. A full‐thickness excisional wound was performed (0d), and the animals were sacrificed 7, 14, and 21 days later. Wound contraction was evaluated by lesion surface measurement at 0d, 7d, 14d, and 21d. The blood pressure of all rats was measured in the beginning and at the each time point of the experiment with a plethysmography method. The wound and normal skin surrounding was formol fixed and paraffin embedded. To evaluate the vessels, an immunohistochemistry for α‐smooth muscle actin was done and stereological parameters were estimated in superficial and deep dermis. At 7d, 14d, and 21d the blood pressure of LNAME group was higher compared with control group (p > 0.001 for all). The wound contraction of LNAME group was slower compared with control group at 14d and 21d (p = 0.004 for both). In superficial dermis, vessels were more dilated in control group compared with LNAME group at 14d and 21d (p = 0.02; p > 0.0001, respectively) and longer in control group compared with LNAME group at 7d and 14d (p = 0.043; p = 0.002, respectively). Deep dermal vessels were more prominent and dilated in control group compared with LNAME group at 21d (p = 0.003; p = 0.0007, respectively), but at 7d, vessels were more dilated in LNAME group compared with control group (p = 0.015). In deep dermis, vessels were longer in control group compared with LNAME group at 14d and 21d (p = 0.002; p = 0.046, respectively). Our results show that nitric oxide inhibition affects the wound contraction and the vascularization pattern, mainly in the later phases of skin wound repair.</abstract><qualityIndicators><score>8.5</score><pdfVersion>1.4</pdfVersion><pdfPageSize>595 x 782 pts</pdfPageSize><refBibsNative>false</refBibsNative><abstractCharCount>1845</abstractCharCount><pdfWordCount>8613</pdfWordCount><pdfCharCount>55105</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>309</abstractWordCount></qualityIndicators><title>Effects of an Inhibitor of Nitric Oxide Synthesis on Skin Wound Repair</title><genre><json:string>abstract</json:string></genre><host><title>Wound Repair and Regeneration</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1524-475X</json:string></doi><issn><json:string>1067-1927</json:string></issn><eissn><json:string>1524-475X</json:string></eissn><publisherId><json:string>WRR</json:string></publisherId><volume>13</volume><issue>1</issue><pages><first>A18</first><last>A18</last><total>1</total></pages><genre><json:string>journal</json:string></genre></host><categories><wos><json:string>science</json:string><json:string>surgery</json:string><json:string>medicine, research & experimental</json:string><json:string>dermatology</json:string><json:string>cell biology</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>dermatology & venereal diseases</json:string></scienceMetrix><inist><json:string>sciences appliquees, technologies et medecines</json:string><json:string>sciences biologiques et medicales</json:string><json:string>sciences medicales</json:string><json:string>hemopathies</json:string></inist></categories><publicationDate>2005</publicationDate><copyrightDate>2005</copyrightDate><doi><json:string>10.1111/j.1067-1927.2005.130117f.x</json:string></doi><id>8AF75EE739A6543EB8CE5D86B4834D4EF3213319</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/8AF75EE739A6543EB8CE5D86B4834D4EF3213319/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/8AF75EE739A6543EB8CE5D86B4834D4EF3213319/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/8AF75EE739A6543EB8CE5D86B4834D4EF3213319/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">Effects of an Inhibitor of Nitric Oxide Synthesis on Skin Wound Repair</title></titleStmt><publicationStmt><publisher>Blackwell Science Inc</publisher><pubPlace>Oxford, UK; 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Malden, USA</pubPlace><date type="published" when="2005-01"></date></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><abstract xml:lang="en" style="main"><p>Considering that nitric oxide (NO) plays an important role on cutaneous wound repair, but its effects have not been defined, an inhibitor of NO synthesis (LNAME) was used. Control group received free water and LNAME group received LNAME (20 mg/kg/day) in drinking water. A full‐thickness excisional wound was performed (0d), and the animals were sacrificed 7, 14, and 21 days later. Wound contraction was evaluated by lesion surface measurement at 0d, 7d, 14d, and 21d. The blood pressure of all rats was measured in the beginning and at the each time point of the experiment with a plethysmography method. The wound and normal skin surrounding was formol fixed and paraffin embedded. To evaluate the vessels, an immunohistochemistry for α‐smooth muscle actin was done and stereological parameters were estimated in superficial and deep dermis. At 7d, 14d, and 21d the blood pressure of LNAME group was higher compared with control group (p < 0.001 for all). The wound contraction of LNAME group was slower compared with control group at 14d and 21d (p = 0.004 for both). In superficial dermis, vessels were more dilated in control group compared with LNAME group at 14d and 21d (p = 0.02; p < 0.0001, respectively) and longer in control group compared with LNAME group at 7d and 14d (p = 0.043; p = 0.002, respectively). Deep dermal vessels were more prominent and dilated in control group compared with LNAME group at 21d (p = 0.003; p = 0.0007, respectively), but at 7d, vessels were more dilated in LNAME group compared with control group (p = 0.015). In deep dermis, vessels were longer in control group compared with LNAME group at 14d and 21d (p = 0.002; p = 0.046, respectively). Our results show that nitric oxide inhibition affects the wound contraction and the vascularization pattern, mainly in the later phases of skin wound repair.</p></abstract><textClass><classCode scheme="tocHeading1">Abstracts ‐ European Tissue Repair Society Focus Meeting</classCode></textClass><langUsage><language ident="EN"></language></langUsage></profileDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/8AF75EE739A6543EB8CE5D86B4834D4EF3213319/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley component found"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Science Inc</publisherName><publisherLoc>Oxford, UK; Malden, USA</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1524-475X</doi><issn type="print">1067-1927</issn><issn type="electronic">1524-475X</issn><idGroup><id type="product" value="WRR"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="WOUND REPAIR REGENERATION">Wound Repair and Regeneration</title></titleGroup></publicationMeta><publicationMeta level="part" position="01101"><doi origin="wiley">10.1111/wrr.2005.13.issue-1</doi><numberingGroup><numbering type="journalVolume" number="13">13</numbering><numbering type="journalIssue" number="1">1</numbering></numberingGroup><coverDate startDate="2005-01">January 2005</coverDate></publicationMeta><publicationMeta level="unit" type="abstract" position="0001800" status="forIssue"><doi origin="wiley">10.1111/j.1067-1927.2005.130117f.x</doi><idGroup><id type="unit" value="WRR130117F"></id></idGroup><countGroup><count type="pageTotal" number="1"></count></countGroup><titleGroup><title type="tocHeading1">Abstracts ‐ European Tissue Repair Society Focus Meeting</title></titleGroup><eventGroup><event type="firstOnline" date="2005-01-17"></event><event type="publishedOnlineFinalForm" date="2005-01-17"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.17 mode:FullText" date="2010-09-08"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-10"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-11-04"></event></eventGroup><numberingGroup><numbering type="pageFirst">A18</numbering><numbering type="pageLast">A18</numbering></numberingGroup><linkGroup><link type="toTypesetVersion" href="file:WRR.WRR130117F.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="0"></count><count type="wordTotal" number="4249"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Effects of an Inhibitor of Nitric Oxide Synthesis on Skin Wound Repair</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>TP</givenNames><familyName>Amadeu</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>A</givenNames><familyName>Desmoulière</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>AMA</givenNames><familyName>Costa</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="BR"><unparsedAffiliation>Histology and Embryology Department, State University of Rio de Janeiro, RJ, Brazil,</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="FR"><unparsedAffiliation>INSERM E0362, Université Victor Segalen, Bordeaux, France</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Considering that nitric oxide (NO) plays an important role on cutaneous wound repair, but its effects have not been defined, an inhibitor of NO synthesis (LNAME) was used. Control group received free water and LNAME group received LNAME (20 mg/kg/day) in drinking water. A full‐thickness excisional wound was performed (0d), and the animals were sacrificed 7, 14, and 21 days later. Wound contraction was evaluated by lesion surface measurement at 0d, 7d, 14d, and 21d. The blood pressure of all rats was measured in the beginning and at the each time point of the experiment with a plethysmography method. The wound and normal skin surrounding was formol fixed and paraffin embedded. To evaluate the vessels, an immunohistochemistry for α‐smooth muscle actin was done and stereological parameters were estimated in superficial and deep dermis. At 7d, 14d, and 21d the blood pressure of LNAME group was higher compared with control group (p < 0.001 for all). The wound contraction of LNAME group was slower compared with control group at 14d and 21d (p = 0.004 for both). In superficial dermis, vessels were more dilated in control group compared with LNAME group at 14d and 21d (p = 0.02; p < 0.0001, respectively) and longer in control group compared with LNAME group at 7d and 14d (p = 0.043; p = 0.002, respectively). Deep dermal vessels were more prominent and dilated in control group compared with LNAME group at 21d (p = 0.003; p = 0.0007, respectively), but at 7d, vessels were more dilated in LNAME group compared with control group (p = 0.015). In deep dermis, vessels were longer in control group compared with LNAME group at 14d and 21d (p = 0.002; p = 0.046, respectively). Our results show that nitric oxide inhibition affects the wound contraction and the vascularization pattern, mainly in the later phases of skin wound repair.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Effects of an Inhibitor of Nitric Oxide Synthesis on Skin Wound Repair</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Effects of an Inhibitor of Nitric Oxide Synthesis on Skin Wound Repair</title></titleInfo><name type="personal"><namePart type="given">TP</namePart><namePart type="family">Amadeu</namePart><affiliation>Histology and Embryology Department, State University of Rio de Janeiro, RJ, Brazil,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Desmoulière</namePart><affiliation>INSERM E0362, Université Victor Segalen, Bordeaux, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">AMA</namePart><namePart type="family">Costa</namePart><affiliation>Histology and Embryology Department, State University of Rio de Janeiro, RJ, Brazil,</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="abstract" displayLabel="abstract"></genre><originInfo><publisher>Blackwell Science Inc</publisher><place><placeTerm type="text">Oxford, UK; Malden, USA</placeTerm></place><dateIssued encoding="w3cdtf">2005-01</dateIssued><copyrightDate encoding="w3cdtf">2005</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="words">4249</extent></physicalDescription><abstract lang="en">Considering that nitric oxide (NO) plays an important role on cutaneous wound repair, but its effects have not been defined, an inhibitor of NO synthesis (LNAME) was used. Control group received free water and LNAME group received LNAME (20 mg/kg/day) in drinking water. A full‐thickness excisional wound was performed (0d), and the animals were sacrificed 7, 14, and 21 days later. Wound contraction was evaluated by lesion surface measurement at 0d, 7d, 14d, and 21d. The blood pressure of all rats was measured in the beginning and at the each time point of the experiment with a plethysmography method. The wound and normal skin surrounding was formol fixed and paraffin embedded. To evaluate the vessels, an immunohistochemistry for α‐smooth muscle actin was done and stereological parameters were estimated in superficial and deep dermis. At 7d, 14d, and 21d the blood pressure of LNAME group was higher compared with control group (p < 0.001 for all). The wound contraction of LNAME group was slower compared with control group at 14d and 21d (p = 0.004 for both). In superficial dermis, vessels were more dilated in control group compared with LNAME group at 14d and 21d (p = 0.02; p < 0.0001, respectively) and longer in control group compared with LNAME group at 7d and 14d (p = 0.043; p = 0.002, respectively). Deep dermal vessels were more prominent and dilated in control group compared with LNAME group at 21d (p = 0.003; p = 0.0007, respectively), but at 7d, vessels were more dilated in LNAME group compared with control group (p = 0.015). In deep dermis, vessels were longer in control group compared with LNAME group at 14d and 21d (p = 0.002; p = 0.046, respectively). Our results show that nitric oxide inhibition affects the wound contraction and the vascularization pattern, mainly in the later phases of skin wound repair.</abstract><relatedItem type="host"><titleInfo><title>Wound Repair and Regeneration</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">1067-1927</identifier><identifier type="eISSN">1524-475X</identifier><identifier type="DOI">10.1111/(ISSN)1524-475X</identifier><identifier type="PublisherID">WRR</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>A18</start><end>A18</end><total>1</total></extent></part></relatedItem><identifier type="istex">8AF75EE739A6543EB8CE5D86B4834D4EF3213319</identifier><identifier type="DOI">10.1111/j.1067-1927.2005.130117f.x</identifier><identifier type="ArticleID">WRR130117F</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Science Inc</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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