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


  • Junli Luo Department of Anesthesiology, Affiliated Hospital of Zunyi Medical University, China
  • Dongdong Li Department of Pain Treatment, Weifang Hospital of Traditional Chinese Medicine, China
  • Song Chen Department of Anesthesiology, Affiliated Hospital of Zunyi Medical University, China
  • Hong Zhang Department of Anesthesiology, Affiliated Hospital of Zunyi Medical University, China
  • Huijun Cai Department of Anesthesiology, Affiliated Hospital of Zunyi Medical University, China



cardiopulmonary bypass, Ischemia-reperfusion, lung apoptosis, PI3K/Akt pathway, Sevoflurane postconditioning


Aims: 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 a control (C group), ischemia/reperfusion (I/R group), sevoflurane postconditioning (S group), and wortmannin group (S+W group). At 10 min after the establishment of CPB, the left pulmonary artery was blocked. When the pulmonary artery was reopened, 2% sevoflurane was administered. Wortmannin was delivered 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 the inferior lobe of the left lung were isolated and subjected to gas analysis, pathological examination, western blot, and TUNEL staining.

Results: No obvious changes were observed in the C group throughout the experiment. The conditions of all treated groups progressively deteriorated, and no difference could be found except in the number of apoptotic cells of T3 between the S+W and I/R groups. At T2, the treated groups showed similar conditions. At T3, the lung function and structure of the S group were improved in I/R and S+W groups. The S group showed the highest p-Akt expression, the lowest cleaved-caspase 3 expression, and apoptotic cell percentage.

Conclusions: Ischemia-reperfusion of the 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.


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How to Cite

Luo, J. ., Li, D., Chen, S., Zhang, H., & Cai, H. (2022). Sevoflurane Postconditioning Inhibits Pulmonary Apoptosis via PI3K/AKT in Dog Cardiopulmonary Bypass Model. The Heart Surgery Forum, 25(3), E374-E380.