Sevoflurane- and Desflurane-induced human myocardial post-conditioning through Phosphatidylinositol-3-kinase/Akt signalling

Background: The role of phosphatidylinositol‐3‐kinase (PI3K) in sevoflurane‐ and desflurane‐induced myocardial post‐conditioning remains unknown. Methods: We recorded isometric contraction of isolated human right atrial trabeculae (oxygenated Tyrode's at 34 °C, stimulation frequency 1 Hz). In all groups, a 30‐min hypoxic period was followed by a 60‐min reoxygenation period. At the onset of reoxygenation, muscles were exposed to 5 min of sevoflurane 1%, 2%, and 3%, and desflurane 3%, 6%, and 9%. In separate groups, sevoflurane 2% and desflurane 6% were administered in the presence of 100 nM wortmannin, a PI3K inhibitor. Recovery of force after the 60‐min reoxygenation period was compared between groups (mean ± SD). Result: As compared with the Control group (49 ± 7% of baseline) PostC by sevoflurane 1%, 2%, and 3% (78 ± 4%, 79 ± 5%, and 85 ± 4% of baseline, respectively) and desflurane 3%, 6%, and 9% (74 ± 5%, 84 ± 4%, and 86 ± 11% of baseline, respectively) enhanced the recovery of force. This effect was abolished in the presence of wortmannin (56 ± 5% of baseline for sevoflurane 2%+wortmannin; 56 ± 3% of baseline for desflurane 6%+wortmannin). Wortmannin alone had no effect on the recovery of force (57 ± 7% of baseline). Conclusion: In vitro, sevoflurane and desflurane post‐conditioned human myocardium against hypoxia through activation of phosphatidylinositol‐3‐kinase.