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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2004-8-9
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pubmed:abstractText |
Maintenance of enterocyte activity during extracellular acidosis requires functional sodium/proton exchangers (NHE), which are present at both basolateral and apical surfaces. Necrotizing enterocolitis is characterized by systemic hypoperfusion, metabolic acidosis, and the apical to basolateral translocation of endotoxin (lipopolysaccharide [LPS]). We hypothesized that LPS differentially impairs NHE activity at the basolateral or apical domains of enterocytes, leading to cellular acidification, and explored the mechanisms involved.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0039-6060
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pubmed:author |
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pubmed:copyrightInfo |
Copyright 2004 Elsevier Inc.
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pubmed:issnType |
Print
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pubmed:volume |
136
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
375-83
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pubmed:meshHeading |
pubmed-meshheading:15300204-Acidosis,
pubmed-meshheading:15300204-Animals,
pubmed-meshheading:15300204-Cells, Cultured,
pubmed-meshheading:15300204-Enterocolitis, Necrotizing,
pubmed-meshheading:15300204-Enterocytes,
pubmed-meshheading:15300204-Hydrogen-Ion Concentration,
pubmed-meshheading:15300204-Lipopolysaccharides,
pubmed-meshheading:15300204-Rats,
pubmed-meshheading:15300204-Sodium-Hydrogen Antiporter
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pubmed:year |
2004
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pubmed:articleTitle |
Endotoxin differentially modulates the basolateral and apical sodium/proton exchangers (NHE) in enterocytes.
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pubmed:affiliation |
Division of Pediatric Surgery, Department of Surgery, Children's Hospital of Pittsburgh, University of Pittsburgh, and the Center of Biologic Imaging, PA 15213, USA.
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pubmed:publicationType |
Journal Article
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