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ID 52343
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Author
Yamamoto, Sumiharu
Okazaki, Mikio
Otani, Shinji
Kakishita, Tomokazu
Yoshida, Osamu
Waki, Naohisa
Toyooka, Shinichi
Sano, Yoshifumi
Abstract
Background: Although lung transplantation from donation after cardiac death (DCD), especially uncontrolled DCD, is limited by warm ischemic periods, the molecular mechanism of warm ischemia-reperfusion-injury (IRI) has not been well elucidated. The purpose of this study was to clarify the particular longitudinal mechanisms of molecular factors involved in warm IRI. Methods: Cold ischemic-time (CIT)-group lungs were retrieved and subjected to 3-h of cold preservation, whereas warm ischemic-time (WIT)-group lungs were retrieved after 3-h of warm ischemia. Orthotopic rat lung transplantation was performed and the grafts were reperfused for 1 or 4-h. The graft functions, gene expression, and activation of inflammatory molecules in the grafts were analyzed. Exhaled-carbon-monoxide-concentration (ExCO-C) was measured during reperfusion. Results: Only the WIT-group showed obvious primary graft dysfunction at 1-h reperfusion, but the graft function was recovered during 4-h reperfusion. Most of pro-inflammatory cytokines and stress-induced molecules showed different expression and activation patterns between CIT and WIT groups. In the WIT-group, the expressions of anti-inflammatory molecules, IL-10 and HO-1, were significantly increased at 1-h reperfusion compared to the CIT-group, and these high levels were maintained through 4-h reperfusion. Furthermore, ExCO-C levels in the WIT-group increased immediately after reperfusion compared to the CIT-group. Conclusions: This study indicates that warm IRI may involve a different mechanism than cold IRI and anti-inflammatory pathways may play important roles in the graft recovery after lung transplantation from uncontrolled DCD.
Keywords
Lung transplantation
Donation after cardiac death
Ischemia reperfusion injury
Warm ischemia
Published Date
2012-03
Publication Title
Transplant Immunology
Volume
volume26
Issue
issue2-3
Start Page
133
End Page
139
ISSN
0966-3274
Content Type
Journal Article
Official Url
http://www.sciencedirect.com/science/article/pii/S0966327411001298
Related Url
http://ousar.lib.okayama-u.ac.jp/metadata/52245
language
英語
Copyright Holders
(C) 2011 Elsevier B.V. All rights reserved.
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Refereed
True
DOI
Web of Sience KeyUT