Sevoflurane Postconditioning Inhibits Pulmonary Apoptosis via PI3K/AKT in Dog Cardiopulmonary Bypass Model

Background: The study aimed to investigate the protective effects and regulatory mechanism of sevoflurane postconditioning (SPC) in pulmonary apoptosis induced by cardiopulmonary bypass (CPB). Methods: : Twenty-four healthy dogs were divided into control (C group), ischemia/reperfusion (I/R group), sevoflurane postconditioning (SPO group) and wortmannin group (S+W group). At 10 min after the establishment of CPB, the left pulmonary artery was blocked. 2% sevoflurane was administrated when the pulmonary artery was reopened. Wortmannin was delivered for 10 min before the pulmonary artery was open. Before thoracotomy was implemented (T1), when the artery was reopened (T2) and 2 h after CPB (T3), blood and inferior lobe of left lung were isolated and subjected to gas analysis, pathological examination, western blot, and TUNEL staining. Results: : No obvious changes were observed in C group throughout the experiment. The conditions of all treated groups progressively deteriorated and no difference could be found except the number of apoptotic cells of T3 between S+W and I/R group. At T2, the treated groups showed similar conditions. At T3, the lung function and structure of S group were improved than I/R and S+W group. S group showed the highest p-Akt expression, the lowest cleaved-caspase 3 expression and apoptotic cell percentage. Conclusions: : Ischemia reperfusion of lung during CPB reduces lung function and injures the pulmonary structure via inducing lung apoptosis. Sevoflurane postconditioning preserves lung function and structure by alleviating apoptosis via activation of PI3K/Akt.