Marked alterations in circulating inflammatory cells during cardiomyopathy development in a magnesium-deficient rat model
Identifieur interne : 001930 ( Istex/Corpus ); précédent : 001929; suivant : 001931Marked alterations in circulating inflammatory cells during cardiomyopathy development in a magnesium-deficient rat model
Auteurs : Joseph Kurantsin-Mills ; Marie M. Cassidy ; Richard E. Stafford ; William B. WeglickiSource :
- British Journal of Nutrition [ 0007-1145 ] ; 1997-11.
Abstract
Rodents fed on a Mg-deficient (Mg-D) diet develop cardiomyopathic lesions, as well as other types of cardiovascular dysfunction. In the rat, inflammatory cell infiltration of the myocardium begins to occur by week 1, and the lesions develop extensively in the third and fourth weeks on the Mg-D diet. Although the aetiologic mechanisms of Mg-D cardiomyopathy are unknown, we have previously reported that once plasma Mg is markedly reduced, one of the earliest molecular markers of the pathophysiological process is elevation of plasma substance P, calcitonin gene-related peptide and prostaglandin E2, followed by histamine and the inflammatory cytokines (interleukin-1, interleukin-6, and tumor necrosis factor-α). In order to evaluate the potential role of specific circulating inflammatory cell subpopulations in the mechanisms underlying pathophysiological changes observed in Mg-deficiency-induced cardiomyopathy, we analysed these cells by flow cytochemistry. Leucocyte subpopulation pools increased progressively in the Mg-D rats. Elevated circulating levels of neutrophils and lymphocytes appeared to contribute to both the acute (week 1–2) and chronic phases (week 3–4) of the inflammatory responses; monocytes, eosinophils, basophils and large unstained cells which are lymphoid in stained smears, on the other hand, increased significantly in the third and fourth weeks and thus contributed to the chronic inflammatory phase. Changes in the circulating leucocyte subpopulations paralleled the chronological progression of the cardiomyopathic lesions, particularly in weeks 3 and 4. Since a pronounced neutrophilia preceded leucocyte infiltration and deposition within the myocardial tissue, modifications of the microvascular barrier may be a prerequisite for cardiomyopathy in this model of neurogenic inflammation.
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DOI: 10.1079/BJN19970200
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Marked alterations in circulating inflammatory cells during cardiomyopathy development in a magnesium-deficient rat model</title><author><name sortKey="Kurantsin Mills, Joseph" sort="Kurantsin Mills, Joseph" uniqKey="Kurantsin Mills J" first="Joseph" last="Kurantsin-Mills">Joseph Kurantsin-Mills</name><affiliation><mods:affiliation>Division of Hematology and Oncology, Department of Medicine, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Physiology, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</mods:affiliation></affiliation></author><author><name sortKey="Cassidy, Marie M" sort="Cassidy, Marie M" uniqKey="Cassidy M" first="Marie M." last="Cassidy">Marie M. Cassidy</name><affiliation><mods:affiliation>Department of Physiology, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</mods:affiliation></affiliation></author><author><name sortKey="Stafford, Richard E" sort="Stafford, Richard E" uniqKey="Stafford R" first="Richard E." last="Stafford">Richard E. Stafford</name><affiliation><mods:affiliation>Division of Experimental Medicine, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</mods:affiliation></affiliation></author><author><name sortKey="Weglicki, William B" sort="Weglicki, William B" uniqKey="Weglicki W" first="William B." last="Weglicki">William B. Weglicki</name><affiliation><mods:affiliation>Division of Experimental Medicine, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:B567730332AC1A0C43B36A97379B24FC2E458BBA</idno><date when="1997" year="1997">1997</date><idno type="doi">10.1079/BJN19970200</idno><idno type="url">https://api.istex.fr/ark:/67375/6GQ-CLXD9SN0-J/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">001930</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">001930</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Marked alterations in circulating inflammatory cells during cardiomyopathy development in a magnesium-deficient rat model</title><author><name sortKey="Kurantsin Mills, Joseph" sort="Kurantsin Mills, Joseph" uniqKey="Kurantsin Mills J" first="Joseph" last="Kurantsin-Mills">Joseph Kurantsin-Mills</name><affiliation><mods:affiliation>Division of Hematology and Oncology, Department of Medicine, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Physiology, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</mods:affiliation></affiliation></author><author><name sortKey="Cassidy, Marie M" sort="Cassidy, Marie M" uniqKey="Cassidy M" first="Marie M." last="Cassidy">Marie M. Cassidy</name><affiliation><mods:affiliation>Department of Physiology, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</mods:affiliation></affiliation></author><author><name sortKey="Stafford, Richard E" sort="Stafford, Richard E" uniqKey="Stafford R" first="Richard E." last="Stafford">Richard E. Stafford</name><affiliation><mods:affiliation>Division of Experimental Medicine, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</mods:affiliation></affiliation></author><author><name sortKey="Weglicki, William B" sort="Weglicki, William B" uniqKey="Weglicki W" first="William B." last="Weglicki">William B. Weglicki</name><affiliation><mods:affiliation>Division of Experimental Medicine, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">British Journal of Nutrition</title><title level="j" type="abbrev">Br J Nutr</title><idno type="ISSN">0007-1145</idno><idno type="eISSN">1475-2662</idno><imprint><publisher>Cambridge University Press</publisher><pubPlace>Cambridge, UK</pubPlace><date type="published" when="1997-11">1997-11</date><biblScope unit="volume">78</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="845">845</biblScope><biblScope unit="page" to="855">855</biblScope></imprint><idno type="ISSN">0007-1145</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0007-1145</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Rodents fed on a Mg-deficient (Mg-D) diet develop cardiomyopathic lesions, as well as other types of cardiovascular dysfunction. In the rat, inflammatory cell infiltration of the myocardium begins to occur by week 1, and the lesions develop extensively in the third and fourth weeks on the Mg-D diet. Although the aetiologic mechanisms of Mg-D cardiomyopathy are unknown, we have previously reported that once plasma Mg is markedly reduced, one of the earliest molecular markers of the pathophysiological process is elevation of plasma substance P, calcitonin gene-related peptide and prostaglandin E2, followed by histamine and the inflammatory cytokines (interleukin-1, interleukin-6, and tumor necrosis factor-α). In order to evaluate the potential role of specific circulating inflammatory cell subpopulations in the mechanisms underlying pathophysiological changes observed in Mg-deficiency-induced cardiomyopathy, we analysed these cells by flow cytochemistry. Leucocyte subpopulation pools increased progressively in the Mg-D rats. Elevated circulating levels of neutrophils and lymphocytes appeared to contribute to both the acute (week 1–2) and chronic phases (week 3–4) of the inflammatory responses; monocytes, eosinophils, basophils and large unstained cells which are lymphoid in stained smears, on the other hand, increased significantly in the third and fourth weeks and thus contributed to the chronic inflammatory phase. Changes in the circulating leucocyte subpopulations paralleled the chronological progression of the cardiomyopathic lesions, particularly in weeks 3 and 4. Since a pronounced neutrophilia preceded leucocyte infiltration and deposition within the myocardial tissue, modifications of the microvascular barrier may be a prerequisite for cardiomyopathy in this model of neurogenic inflammation.</div></front></TEI><istex><corpusName>cambridge</corpusName><author><json:item><name>Joseph Kurantsin-Mills</name><affiliations><json:string>Division of Hematology and Oncology, Department of Medicine, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</json:string><json:string>Department of Physiology, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</json:string></affiliations></json:item><json:item><name>Marie M. Cassidy</name><affiliations><json:string>Department of Physiology, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</json:string></affiliations></json:item><json:item><name>Richard E. Stafford</name><affiliations><json:string>Division of Experimental Medicine, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</json:string></affiliations></json:item><json:item><name>William B. Weglicki</name><affiliations><json:string>Division of Experimental Medicine, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Magnesium</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Neutrophilia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Inflammatory cells</value></json:item></subject><articleId><json:string>00187</json:string></articleId><arkIstex>ark:/67375/6GQ-CLXD9SN0-J</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>research-article</json:string></originalGenre><abstract>Rodents fed on a Mg-deficient (Mg-D) diet develop cardiomyopathic lesions, as well as other types of cardiovascular dysfunction. In the rat, inflammatory cell infiltration of the myocardium begins to occur by week 1, and the lesions develop extensively in the third and fourth weeks on the Mg-D diet. Although the aetiologic mechanisms of Mg-D cardiomyopathy are unknown, we have previously reported that once plasma Mg is markedly reduced, one of the earliest molecular markers of the pathophysiological process is elevation of plasma substance P, calcitonin gene-related peptide and prostaglandin E2, followed by histamine and the inflammatory cytokines (interleukin-1, interleukin-6, and tumor necrosis factor-α). In order to evaluate the potential role of specific circulating inflammatory cell subpopulations in the mechanisms underlying pathophysiological changes observed in Mg-deficiency-induced cardiomyopathy, we analysed these cells by flow cytochemistry. Leucocyte subpopulation pools increased progressively in the Mg-D rats. Elevated circulating levels of neutrophils and lymphocytes appeared to contribute to both the acute (week 1–2) and chronic phases (week 3–4) of the inflammatory responses; monocytes, eosinophils, basophils and large unstained cells which are lymphoid in stained smears, on the other hand, increased significantly in the third and fourth weeks and thus contributed to the chronic inflammatory phase. Changes in the circulating leucocyte subpopulations paralleled the chronological progression of the cardiomyopathic lesions, particularly in weeks 3 and 4. Since a pronounced neutrophilia preceded leucocyte infiltration and deposition within the myocardial tissue, modifications of the microvascular barrier may be a prerequisite for cardiomyopathy in this model of neurogenic inflammation.</abstract><qualityIndicators><score>8.907</score><pdfWordCount>3907</pdfWordCount><pdfCharCount>24535</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>11</pdfPageCount><pdfPageSize>486 x 702 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>250</abstractWordCount><abstractCharCount>1828</abstractCharCount><keywordCount>3</keywordCount></qualityIndicators><title>Marked alterations in circulating inflammatory cells during cardiomyopathy development in a magnesium-deficient rat model</title><pii><json:string>S0007114597001876</json:string></pii><genre><json:string>research-article</json:string></genre><host><title>British Journal of Nutrition</title><language><json:string>unknown</json:string></language><issn><json:string>0007-1145</json:string></issn><eissn><json:string>1475-2662</json:string></eissn><publisherId><json:string>BJN</json:string></publisherId><volume>78</volume><issue>5</issue><pages><first>845</first><last>855</last><total>11</total></pages><genre><json:string>journal</json:string></genre></host><ark><json:string>ark:/67375/6GQ-CLXD9SN0-J</json:string></ark><categories><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string></inist></categories><publicationDate>1997</publicationDate><copyrightDate>1997</copyrightDate><doi><json:string>10.1079/BJN19970200</json:string></doi><id>B567730332AC1A0C43B36A97379B24FC2E458BBA</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/6GQ-CLXD9SN0-J/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/6GQ-CLXD9SN0-J/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/6GQ-CLXD9SN0-J/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Marked alterations in circulating inflammatory cells during cardiomyopathy development in a magnesium-deficient rat model</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher scheme="https://scientific-publisher.data.istex.fr">Cambridge University Press</publisher><pubPlace>Cambridge, UK</pubPlace><availability><licence><p>Copyright © The Nutrition Society 1997</p></licence><p scheme="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-G3RCRD03-V">cambridge</p></availability><date>1997</date></publicationStmt><notesStmt><note type="research-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</note><note type="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Marked alterations in circulating inflammatory cells during cardiomyopathy development in a magnesium-deficient rat model</title><author xml:id="author-0000"><persName><forename type="first">Joseph</forename><surname>Kurantsin-Mills</surname></persName><affiliation>Division of Hematology and Oncology, Department of Medicine, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</affiliation><affiliation>Department of Physiology, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Marie M.</forename><surname>Cassidy</surname></persName><affiliation>Department of Physiology, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</affiliation></author><author xml:id="author-0002"><persName><forename type="first">Richard E.</forename><surname>Stafford</surname></persName><affiliation>Division of Experimental Medicine, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</affiliation></author><author xml:id="author-0003"><persName><forename type="first">William B.</forename><surname>Weglicki</surname></persName><affiliation>Division of Experimental Medicine, Department of Medicine, The George Washington University Medical Center, Washington, DC 20037, USA</affiliation></author><idno type="istex">B567730332AC1A0C43B36A97379B24FC2E458BBA</idno><idno type="ark">ark:/67375/6GQ-CLXD9SN0-J</idno><idno type="DOI">10.1079/BJN19970200</idno><idno type="PII">S0007114597001876</idno><idno type="article-id">00187</idno></analytic><monogr><title level="j">British Journal of Nutrition</title><title level="j" type="abbrev">Br J Nutr</title><idno type="pISSN">0007-1145</idno><idno type="eISSN">1475-2662</idno><idno type="publisher-id">BJN</idno><imprint><publisher>Cambridge University Press</publisher><pubPlace>Cambridge, UK</pubPlace><date type="published" when="1997-11"></date><biblScope unit="volume">78</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="845">845</biblScope><biblScope unit="page" to="855">855</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1997</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en" style="normal"><p>Rodents fed on a Mg-deficient (Mg-D) diet develop cardiomyopathic lesions, as well as other types of cardiovascular dysfunction. In the rat, inflammatory cell infiltration of the myocardium begins to occur by week 1, and the lesions develop extensively in the third and fourth weeks on the Mg-D diet. Although the aetiologic mechanisms of Mg-D cardiomyopathy are unknown, we have previously reported that once plasma Mg is markedly reduced, one of the earliest molecular markers of the pathophysiological process is elevation of plasma substance P, calcitonin gene-related peptide and prostaglandin E2, followed by histamine and the inflammatory cytokines (interleukin-1, interleukin-6, and tumor necrosis factor-α). In order to evaluate the potential role of specific circulating inflammatory cell subpopulations in the mechanisms underlying pathophysiological changes observed in Mg-deficiency-induced cardiomyopathy, we analysed these cells by flow cytochemistry. Leucocyte subpopulation pools increased progressively in the Mg-D rats. Elevated circulating levels of neutrophils and lymphocytes appeared to contribute to both the acute (week 1–2) and chronic phases (week 3–4) of the inflammatory responses; monocytes, eosinophils, basophils and large unstained cells which are lymphoid in stained smears, on the other hand, increased significantly in the third and fourth weeks and thus contributed to the chronic inflammatory phase. Changes in the circulating leucocyte subpopulations paralleled the chronological progression of the cardiomyopathic lesions, particularly in weeks 3 and 4. Since a pronounced neutrophilia preceded leucocyte infiltration and deposition within the myocardial tissue, modifications of the microvascular barrier may be a prerequisite for cardiomyopathy in this model of neurogenic inflammation.</p></abstract><textClass><keywords scheme="keyword"><list><head></head><item><term>Magnesium</term></item><item><term>Neutrophilia</term></item><item><term>Inflammatory cells</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1997-11">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6GQ-CLXD9SN0-J/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus cambridge not found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.2 20060430//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="research-article" dtd-version="2.2" xml:lang="EN"><front><journal-meta><journal-id journal-id-type="publisher-id">BJN</journal-id><journal-title>British Journal of Nutrition</journal-title><abbrev-journal-title>Br J Nutr</abbrev-journal-title><issn pub-type="ppub">0007-1145</issn><issn pub-type="epub">1475-2662</issn><publisher><publisher-name>Cambridge University Press</publisher-name><publisher-loc>Cambridge, UK</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.1079/BJN19970200</article-id><article-id pub-id-type="pii">S0007114597001876</article-id><article-id pub-id-type="publisher-id">00187</article-id><title-group><article-title>Marked alterations in circulating inflammatory cells during cardiomyopathy development in a magnesium-deficient rat model</article-title><alt-title alt-title-type="left-running">J. KURANTSIN-MILLS <italic>ET AL.</italic></alt-title><alt-title alt-title-type="right-running">INFLAMMATORY CELLS IN MAGNESIUM DEFICIENCY</alt-title></title-group><contrib-group><contrib><name name-style="western"><surname>Kurantsin-Mills</surname><given-names>Joseph</given-names></name><xref ref-type="aff" rid="aff1"><sup>1</sup></xref><xref ref-type="aff" rid="aff2"><sup>2</sup></xref></contrib><contrib><name name-style="western"><surname>Cassidy</surname><given-names>Marie M.</given-names></name><xref ref-type="aff" rid="aff2"><sup>2</sup></xref></contrib><contrib><name name-style="western"><surname>Stafford</surname><given-names>Richard E.</given-names></name><xref ref-type="aff" rid="aff3"><sup>3</sup></xref></contrib><contrib><name name-style="western"><surname>Weglicki</surname><given-names>William B.</given-names></name><xref ref-type="aff" rid="aff3"><sup>3</sup></xref></contrib></contrib-group><aff id="aff1"><label><sup>1</sup></label> <addr-line>Division of Hematology and Oncology</addr-line>, <addr-line>Department of Medicine</addr-line>, <addr-line>Department of Medicine</addr-line>, <institution>The George Washington University Medical Center</institution>, <addr-line>Washington</addr-line>, <addr-line>DC 20037</addr-line>, <country>USA</country></aff><aff id="aff2"><label><sup>2</sup></label> <addr-line>Department of Physiology</addr-line>, <addr-line>Department of Medicine</addr-line>, <institution>The George Washington University Medical Center</institution>, <addr-line>Washington</addr-line>, <addr-line>DC 20037</addr-line>, <country>USA</country></aff><aff id="aff3"><label><sup>3</sup></label> <addr-line>Division of Experimental Medicine</addr-line>, <addr-line>Department of Medicine</addr-line>, <institution>The George Washington University Medical Center</institution>, <addr-line>Washington</addr-line>, <addr-line>DC 20037</addr-line>, <country>USA</country></aff><pub-date pub-type="ppub"><month>11</month><year>1997</year></pub-date><volume>78</volume><issue>5</issue><fpage seq="17">845</fpage><lpage>855</lpage><history><date date-type="received"><day>04</day><month>12</month><year>1996</year></date><date date-type="rev-recd"><day>21</day><month>04</month><year>1997</year></date><date date-type="accepted"><day>09</day><month>05</month><year>1997</year></date></history><permissions><copyright-statement>Copyright © The Nutrition Society 1997</copyright-statement><copyright-year>1997</copyright-year><copyright-holder>The Nutrition Society</copyright-holder></permissions><abstract abstract-type="normal"><p>Rodents fed on a Mg-deficient (Mg-D) diet develop cardiomyopathic lesions, as well as other types of cardiovascular dysfunction. In the rat, inflammatory cell infiltration of the myocardium begins to occur by week 1, and the lesions develop extensively in the third and fourth weeks on the Mg-D diet. Although the aetiologic mechanisms of Mg-D cardiomyopathy are unknown, we have previously reported that once plasma Mg is markedly reduced, one of the earliest molecular markers of the pathophysiological process is elevation of plasma substance P, calcitonin gene-related peptide and prostaglandin E<sub>2</sub>, followed by histamine and the inflammatory cytokines (interleukin-1, interleukin-6, and tumor necrosis factor-α). In order to evaluate the potential role of specific circulating inflammatory cell subpopulations in the mechanisms underlying pathophysiological changes observed in Mg-deficiency-induced cardiomyopathy, we analysed these cells by flow cytochemistry. Leucocyte subpopulation pools increased progressively in the Mg-D rats. Elevated circulating levels of neutrophils and lymphocytes appeared to contribute to both the acute (week 1–2) and chronic phases (week 3–4) of the inflammatory responses; monocytes, eosinophils, basophils and large unstained cells which are lymphoid in stained smears, on the other hand, increased significantly in the third and fourth weeks and thus contributed to the chronic inflammatory phase. Changes in the circulating leucocyte subpopulations paralleled the chronological progression of the cardiomyopathic lesions, particularly in weeks 3 and 4. Since a pronounced neutrophilia preceded leucocyte infiltration and deposition within the myocardial tissue, modifications of the microvascular barrier may be a prerequisite for cardiomyopathy in this model of neurogenic inflammation.</p></abstract><kwd-group kwd-group-type=""><kwd>Magnesium</kwd><kwd>Neutrophilia</kwd><kwd>Inflammatory cells</kwd></kwd-group><counts><page-count count="11"></page-count></counts><custom-meta-wrap><custom-meta><meta-name>pdf</meta-name><meta-value>S0007114597001876a.pdf</meta-value></custom-meta></custom-meta-wrap><custom-meta-wrap><custom-meta><meta-name>dispart</meta-name><meta-value>General Nutrition</meta-value></custom-meta></custom-meta-wrap></article-meta></front><back><ref-list><title>REFERENCES</title><ref><citation citation-type="book" id="ref001"><name name-style="western"><surname>Aikawa</surname><given-names>J. 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In the rat, inflammatory cell infiltration of the myocardium begins to occur by week 1, and the lesions develop extensively in the third and fourth weeks on the Mg-D diet. Although the aetiologic mechanisms of Mg-D cardiomyopathy are unknown, we have previously reported that once plasma Mg is markedly reduced, one of the earliest molecular markers of the pathophysiological process is elevation of plasma substance P, calcitonin gene-related peptide and prostaglandin E2, followed by histamine and the inflammatory cytokines (interleukin-1, interleukin-6, and tumor necrosis factor-α). In order to evaluate the potential role of specific circulating inflammatory cell subpopulations in the mechanisms underlying pathophysiological changes observed in Mg-deficiency-induced cardiomyopathy, we analysed these cells by flow cytochemistry. Leucocyte subpopulation pools increased progressively in the Mg-D rats. Elevated circulating levels of neutrophils and lymphocytes appeared to contribute to both the acute (week 1–2) and chronic phases (week 3–4) of the inflammatory responses; monocytes, eosinophils, basophils and large unstained cells which are lymphoid in stained smears, on the other hand, increased significantly in the third and fourth weeks and thus contributed to the chronic inflammatory phase. Changes in the circulating leucocyte subpopulations paralleled the chronological progression of the cardiomyopathic lesions, particularly in weeks 3 and 4. Since a pronounced neutrophilia preceded leucocyte infiltration and deposition within the myocardial tissue, modifications of the microvascular barrier may be a prerequisite for cardiomyopathy in this model of neurogenic inflammation.</abstract><subject><genre></genre><topic>Magnesium</topic><topic>Neutrophilia</topic><topic>Inflammatory cells</topic></subject><relatedItem type="host"><titleInfo><title>British Journal of Nutrition</title></titleInfo><titleInfo type="abbreviated"><title>Br J Nutr</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><identifier type="ISSN">0007-1145</identifier><identifier type="eISSN">1475-2662</identifier><identifier type="PublisherID">BJN</identifier><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>78</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>845</start><end>855</end><total>11</total></extent></part></relatedItem><identifier type="istex">B567730332AC1A0C43B36A97379B24FC2E458BBA</identifier><identifier type="ark">ark:/67375/6GQ-CLXD9SN0-J</identifier><identifier type="DOI">10.1079/BJN19970200</identifier><identifier type="PII">S0007114597001876</identifier><identifier type="ArticleID">00187</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © The Nutrition Society 1997</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-G3RCRD03-V">cambridge</recordContentSource><recordOrigin>Copyright © The Nutrition Society 1997</recordOrigin></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6GQ-CLXD9SN0-J/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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