Objective To evaluate the role of PI3K-Akt-HIF-1α signaling pathway in dexmedetomidine-induced reduction of damage to the unventilated lung during one-lung ventilation (OLV) in rats. Methods Forty adult male Sprague-Dawley rats, weighing 250-350 g, were randomly divided into 4 groups (n=10 each) using a random number table: two-lung ventilation (TLV) group, OLV + normal saline group (group OLV), OLV + dexmedetomidine group (group D), and OLV + dexmedetomidine + LY294002 group (group DL). Bilateral lungs were ventilated for 2.5 h in group TLV, and the right lung was ventilated for 2 h followed by 0.5 h TLV in the other groups.The rats were sacrificed, the left lung was removed for determination of wet to dry lung weight ratio (W/D ratio), and expression of phosphorylated Akt (p-Akt) and hypoxia-inducible factor-1 alpha (HIF-1α) (by Western blot). Results Compared with group TLV, W/D ratio was significantly increased, the expression of p-Akt was down-regulated, and the expression of HIF-1α was up-regulated in the other three groups (P<0.05). Compared with group OLV, W/D ratio was significantly decreased, and the expression of p-Akt and HIF-1α was up-regulated in D and DL groups (P<0.05). Compared with group DL, W/D ratio was significantly decreased, and the expression of p-Akt and HIF-1α was up-regulated in group D (P<0.05). Conclusion PI3K-Akt-HIF-1α signaling pathway is involved in dexmedetomidine-induced reduction of damage to the unventilated lung during OLV in rats. Key words: 1-Phosphatidylinositol 3-kinase; Protein-serine-threonine kinases; Hypoxia-indu-cible factor 1, alpha subunit; Dexmedetomidine; Respiration, artificial; Respiratory distress syndrome, adult
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