| pubmed-article:18552698 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18552698 | lifeskim:mentions | umls-concept:C0876973 | lld:lifeskim |
| pubmed-article:18552698 | lifeskim:mentions | umls-concept:C0273115 | lld:lifeskim |
| pubmed-article:18552698 | lifeskim:mentions | umls-concept:C0001127 | lld:lifeskim |
| pubmed-article:18552698 | lifeskim:mentions | umls-concept:C1457868 | lld:lifeskim |
| pubmed-article:18552698 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
| pubmed-article:18552698 | lifeskim:mentions | umls-concept:C2936404 | lld:lifeskim |
| pubmed-article:18552698 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:18552698 | pubmed:dateCreated | 2008-7-2 | lld:pubmed |
| pubmed-article:18552698 | pubmed:abstractText | Hypercapnic acidosis is commonly permitted in patients with acute respiratory distress syndrome during the use of protective ventilation strategies. Hypercapnic acidosis is also a common complication of multiple lung diseases and is associated with a poor prognosis, although the mechanisms by which it leads to increased mortality is not known. Previous studies using noninfective models of lung injury show that acute (<6 hrs) hypercapnic acidosis reduced lung damage by an anti-inflammatory effect. We hypothesized that this anti-inflammatory effect would be detrimental in vivo in the presence of untreated bacterial infection and sustained hypercapnia (>48 hrs) and, furthermore, that if bacterial reproduction were controlled by antibiotic therapy, then the anti-inflammatory effects of hypercapnic acidosis would no longer prove detrimental. | lld:pubmed |
| pubmed-article:18552698 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18552698 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18552698 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18552698 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:18552698 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18552698 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:18552698 | pubmed:issn | 1530-0293 | lld:pubmed |
| pubmed-article:18552698 | pubmed:author | pubmed-author:McLoughlinPau... | lld:pubmed |
| pubmed-article:18552698 | pubmed:author | pubmed-author:LaffeyJohn... | lld:pubmed |
| pubmed-article:18552698 | pubmed:author | pubmed-author:HopkinsNatali... | lld:pubmed |
| pubmed-article:18552698 | pubmed:author | pubmed-author:O'ConnorClare... | lld:pubmed |
| pubmed-article:18552698 | pubmed:author | pubmed-author:O'BrienSorcaS | lld:pubmed |
| pubmed-article:18552698 | pubmed:author | pubmed-author:O'CroininDona... | lld:pubmed |
| pubmed-article:18552698 | pubmed:author | pubmed-author:NicholAlistai... | lld:pubmed |
| pubmed-article:18552698 | pubmed:author | pubmed-author:BoylanJohnJ | lld:pubmed |
| pubmed-article:18552698 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18552698 | pubmed:volume | 36 | lld:pubmed |
| pubmed-article:18552698 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18552698 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18552698 | pubmed:pagination | 2128-35 | lld:pubmed |
| pubmed-article:18552698 | pubmed:meshHeading | pubmed-meshheading:18552698... | lld:pubmed |
| pubmed-article:18552698 | pubmed:meshHeading | pubmed-meshheading:18552698... | lld:pubmed |
| pubmed-article:18552698 | pubmed:meshHeading | pubmed-meshheading:18552698... | lld:pubmed |
| pubmed-article:18552698 | pubmed:meshHeading | pubmed-meshheading:18552698... | lld:pubmed |
| pubmed-article:18552698 | pubmed:meshHeading | pubmed-meshheading:18552698... | lld:pubmed |
| pubmed-article:18552698 | pubmed:meshHeading | pubmed-meshheading:18552698... | lld:pubmed |
| pubmed-article:18552698 | pubmed:meshHeading | pubmed-meshheading:18552698... | lld:pubmed |
| pubmed-article:18552698 | pubmed:meshHeading | pubmed-meshheading:18552698... | lld:pubmed |
| pubmed-article:18552698 | pubmed:meshHeading | pubmed-meshheading:18552698... | lld:pubmed |
| pubmed-article:18552698 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18552698 | pubmed:articleTitle | Sustained hypercapnic acidosis during pulmonary infection increases bacterial load and worsens lung injury. | lld:pubmed |
| pubmed-article:18552698 | pubmed:affiliation | School of Medicine and Medical Sciences, Conway Institute, University College Dublin, Ireland. | lld:pubmed |
| pubmed-article:18552698 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18552698 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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