論文

査読有り
2013年1月

Inhalation of carbon monoxide following resuscitation ameliorates hemorrhagic shock-induced lung injury

MOLECULAR MEDICINE REPORTS
  • Susumu Kawanishi
  • ,
  • Toru Takahashi
  • ,
  • Hiroshi Morimatsu
  • ,
  • Hiroko Shimizu
  • ,
  • Emiko Omori
  • ,
  • Kenji Sato
  • ,
  • Masaki Matsumi
  • ,
  • Shigeru Maeda
  • ,
  • Atsunori Nakao
  • ,
  • Kiyoshi Morita

7
1
開始ページ
3
終了ページ
10
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.3892/mmr.2012.1173
出版者・発行元
SPANDIDOS PUBL LTD

Even after successful resuscitation, hemorrhagic shock frequently causes pulmonary inflammation that induces acute lung injury (ALI). We previously demonstrated that when CO is inhaled at a low concentration both prior to and following hemorrhagic shock and resuscitation (HSR) it ameliorates HSR-induced ALI in rats due to its anti-inflammatory effects. In the present study, we administered CO to the same model of ALI only after resuscitation and examined whether it exerted a therapeutic effect without adverse events on HSR-induced ALI, since treatment of animals with CO prior to HSR did not prevent lung injury. HSR were induced by bleeding animals to achieve a mean arterial pressure of 30 mmHg for I h followed by resuscitation with the removed blood. HSR resulted in the upregulation of inflammatory gene expression and increased the rate of apoptotic cell death in the lungs. This was determined from an observed increase in the number of cells positive for transferase-mediated dUTP-fluorescein isothiocyanate (FITC), nick-end labeling staining and activated caspase-3. HSR also resulted in prominent histopathological damage, including congestion, edema, cellular infiltration and hemorrhage. By contrast, CO inhalation for 3 h following resuscitation significantly ameliorated these inflammatory events, demonstrated by reduced histological damage, inflammatory mediators and apoptotic cell death. The protective effects of CO against lung injury were notably associated with an increase in the protein expression level of peroxisome proliferator-activated receptor (PPAR)-gamma, an anti-inflammatory transcriptional regulator in the lung. Moreover, CO inhalation did not affect the hemodynamic status or tissue oxygenation during HSR. These findings suggest that inhalation of CO at a low concentration exerts a potent therapeutic effect against HSR-induced ALI and attenuates the inflammatory cascade by increasing PPAR-gamma protein expression.

Web of Science ® 被引用回数 : 14

リンク情報
DOI
https://doi.org/10.3892/mmr.2012.1173
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/23138173
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000312238000001&DestApp=WOS_CPL

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