• L Zhu, S Lemoine, G Babatasi, O Lepage, M Massetti, J-L Gérard, and J-L Hanouz.
• Laboratoire d'Anesthesiologie et de Physiologie Cellulaire, Centre Hospitalier Régional, Caen, France.
• Acta Anaesthesiol Scand. 2009 Aug 1; 53 (7): 949-56.

BackgroundThe role of phosphatidylinositol-3-kinase (PI3K) in sevoflurane- and desflurane-induced myocardial post-conditioning remains unknown.MethodsWe recorded isometric contraction of isolated human right atrial trabeculae (oxygenated Tyrode's at 34 degrees 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).ResultAs 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).ConclusionIn vitro, sevoflurane and desflurane post-conditioned human myocardium against hypoxia through activation of phosphatidylinositol-3-kinase.

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