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    <subfield code="2">doi</subfield>
    <subfield code="a">10.1111/nmo.14639</subfield>
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    <subfield code="2">sideral</subfield>
    <subfield code="a">134329</subfield>
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  <datafield tag="037" ind1=" " ind2=" ">
    <subfield code="a">ART-2023-134329</subfield>
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  <datafield tag="041" ind1=" " ind2=" ">
    <subfield code="a">eng</subfield>
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  <datafield tag="100" ind1=" " ind2=" ">
    <subfield code="a">Castro, Marta</subfield>
    <subfield code="u">Universidad de Zaragoza</subfield>
    <subfield code="0">(orcid)0000-0001-8584-3979</subfield>
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  <datafield tag="245" ind1=" " ind2=" ">
    <subfield code="a">Radiographic and histopathological study of gastrointestinal dysmotility in lipopolysaccharide-induced sepsis in the rat</subfield>
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  <datafield tag="260" ind1=" " ind2=" ">
    <subfield code="c">2023</subfield>
  </datafield>
  <datafield tag="506" ind1="0" ind2=" ">
    <subfield code="a">Access copy available to the general public</subfield>
    <subfield code="f">Unrestricted</subfield>
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  <datafield tag="520" ind1="3" ind2=" ">
    <subfield code="a">AbstractSepsis is a highly incident condition in which a cascade of proinflammatory cytokines is involved. One of its most frequent consequences is ileus, which can increase mortality. Animal models such as that induced by systemic administration of lipopolysaccharide (LPS) are useful to deeply evaluate this condition. The effects of sepsis on the gastrointestinal (GI) tract have been explored but, to our knowledge, in vivo studies showing the motor and histopathological consequences of endotoxemia in an integrated way are lacking. Our aim was to study in rats the effects of sepsis on GI motility, using radiographic methods, and to assess histological damage in several organs.MethodsMale rats were intraperitoneally injected with saline or E. coli LPS at 0.1, 1, or 5 mg kg−1. Barium sulfate was intragastrically administered, and X‐rays were performed 0–24 h afterwards. Several organs were collected for organography, histopathology, and immunohistochemistry studies.Key ResultsAll LPS doses caused gastroparesia, whereas changes in intestinal motility were dose‐and time‐dependent, with an initial phase of hypermotility followed by paralytic ileus. Lung, liver, stomach, ileum, and colon (but not spleen or kidneys) were damaged, and density of neutrophils and activated M2 macrophages and expression of cyclooxygenase 2 were increased in the colon 24 h after LPS 5 mg kg−1.Conclusions and InferencesUsing radiographic, noninvasive methods for the first time, we show that systemic LPS causes dose‐, time‐, and organ‐dependent GI motor effects. Sepsis‐induced GI dysmotility is a complex condition whose management needs to take its time‐dependent changes into account.</subfield>
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    <subfield code="9">info:eu-repo/grantAgreement/ES/DGA/B04-17R</subfield>
    <subfield code="9">info:eu-repo/grantAgreement/ES/MICINN/SAF2012-40075-C02-01</subfield>
    <subfield code="9">info:eu-repo/grantAgreement/ES/MINECO/AGL2017-82987-R</subfield>
    <subfield code="9">info:eu-repo/grantAgreement/ES/MINECO/SAF2017-83120-C2-1-R</subfield>
    <subfield code="9">info:eu-repo/grantAgreement/ES/UZ/JIUZ-2015-BIO-02</subfield>
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    <subfield code="9">info:eu-repo/semantics/openAccess</subfield>
    <subfield code="a">by-nc</subfield>
    <subfield code="u">http://creativecommons.org/licenses/by-nc/3.0/es/</subfield>
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    <subfield code="a">3.5</subfield>
    <subfield code="b">2023</subfield>
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    <subfield code="a">CLINICAL NEUROLOGY</subfield>
    <subfield code="b">70 / 280 = 0.25</subfield>
    <subfield code="c">2023</subfield>
    <subfield code="d">Q1</subfield>
    <subfield code="e">T1</subfield>
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    <subfield code="a">NEUROSCIENCES</subfield>
    <subfield code="b">110 / 310 = 0.355</subfield>
    <subfield code="c">2023</subfield>
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    <subfield code="e">T2</subfield>
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    <subfield code="a">GASTROENTEROLOGY &amp; HEPATOLOGY</subfield>
    <subfield code="b">43 / 143 = 0.301</subfield>
    <subfield code="c">2023</subfield>
    <subfield code="d">Q2</subfield>
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    <subfield code="a">1.312</subfield>
    <subfield code="b">2023</subfield>
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  <datafield tag="593" ind1=" " ind2=" ">
    <subfield code="a">Endocrine and Autonomic Systems</subfield>
    <subfield code="c">2023</subfield>
    <subfield code="d">Q1</subfield>
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  <datafield tag="593" ind1=" " ind2=" ">
    <subfield code="a">Physiology</subfield>
    <subfield code="c">2023</subfield>
    <subfield code="d">Q1</subfield>
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  <datafield tag="593" ind1=" " ind2=" ">
    <subfield code="a">Gastroenterology</subfield>
    <subfield code="c">2023</subfield>
    <subfield code="d">Q1</subfield>
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    <subfield code="a">7.8</subfield>
    <subfield code="b">2023</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Valero, Marta Sofía</subfield>
    <subfield code="u">Universidad de Zaragoza</subfield>
    <subfield code="0">(orcid)0000-0002-2231-7565</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">López-Tofiño, Yolanda</subfield>
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    <subfield code="a">López-Gómez, Laura</subfield>
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    <subfield code="a">Girón, Rocío</subfield>
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    <subfield code="a">Martín-Fontelles, María Isabel</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Uranga, José A.</subfield>
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  <datafield tag="700" ind1=" " ind2=" ">
    <subfield code="a">Abalo, Raquel</subfield>
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  <datafield tag="710" ind1="2" ind2=" ">
    <subfield code="1">1012</subfield>
    <subfield code="2">410</subfield>
    <subfield code="a">Universidad de Zaragoza</subfield>
    <subfield code="b">Dpto. Farmac.Fisiol.y Med.L.F.</subfield>
    <subfield code="c">Área Fisiología</subfield>
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  <datafield tag="773" ind1=" " ind2=" ">
    <subfield code="g">35, 10 (2023), e14639 [15 pp]</subfield>
    <subfield code="p">Neurogastroenterol. motil.</subfield>
    <subfield code="t">NEUROGASTROENTEROLOGY AND MOTILITY</subfield>
    <subfield code="x">1350-1925</subfield>
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    <subfield code="s">4378878</subfield>
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