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Receptor for Advanced Glycation End Products Involved in Lung Ischemia Reperfusion Injury in Cardiopulmonary Bypass Attenuated by Controlled Oxygen Reperfusion in a Canine Model
Author(s) -
Jian Rong,
Sheng Ye,
Mengya Liang,
Guangxian Chen,
Hai Liu,
Jinxin Zhang,
Zhongkai Wu
Publication year - 2013
Publication title -
asaio journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.961
H-Index - 66
eISSN - 1538-943X
pISSN - 1058-2916
DOI - 10.1097/mat.0b013e318290504e
Subject(s) - cardiopulmonary bypass , medicine , reperfusion injury , rage (emotion) , hmgb1 , ischemia , lung , glycation , anesthesia , hyperoxia , receptor , biology , neuroscience
Controlled oxygen reperfusion could protect the lung against ischemia-reperfusion injury in cardiopulmonary bypass (CPB) by downregulating high mobility group box 1 (HMGB1), a high affinity receptor of HMGB1. This study investigated the effect of controlled oxygen reperfusion on receptor for advanced glycation end products (RAGE) expression and its downstream effects on lung ischemia-reperfusion injury. Fourteen canines received CPB with 60 minutes of aortic clamping and cardioplegic arrest followed by 90 minutes of reperfusion. Animals were randomized to receive 80% FiO2 during the entire procedure (control group) or to a test group receiving a controlled oxygen reperfusion protocol. Pathologic changes in lung tissues, RAGE expression, serum interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) were evaluated. The lung pathologic scores after 25 and 90 minutes of reperfusion were significantly lower in the test group compared with the control group (p < 0.001). RAGE expression, TNF-α, and IL-6 were downregulated by controlled oxygen treatment (p < 0.001). RAGE might be involved in the lung ischemia-reperfusion injury in canine model of CPB, which was downregulated by controlled oxygen reperfusion.

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