Effects of sevoflurane or ischemic preconditioning on the expression of ERK and CaM during lung ischemia-reperfusion in rats

Objectlve To investigate the effects of sevoflurane or ischemic preconditioning on the expression of extracellular signal-regulated kinase （ERK） and calmodulin （CaM） during lung ischemia-reperfusion （I/R）in rats. Methods Twenty-four male SD rats weighing 270-320 g were randomly divided into 4 groups （ n = 6each）： sham operation group （group S）, group I/R, ischemic preconditioning group （group IP）, and sevoflurane preconditioning group （group SP）. In group S, the hilum of the left lung was dissociated after thoracotomy but not occluded. In group I/R, lung I/R was produced by occlusion of the hilum of the left lung for 45 min followed by 120 min of reperfusion. In group IP, the hilum of the left lung was occluded for 5 min and unclamped for 5 min for 2 times before the model was established. In group SP, sevoflurane was inhaled for 30 min at the end-tidal concentration of 2.1% before lung ischemia. All rats were sacrificed at 120 min of reperfusion and the lung tissues were taken for determination of the contents of TNF-α and IL-6 by ELISA and the expression of ERK mRNA and CaM mRNA by RT-PCR. Results Compared with group S, the contents of TNF-α and IL-6 and the expression of ERK mRNA and CaM mRNA were significantly increased in group I/R, IP and SP （ P 〈 0.05）. Compared with group I/R, the contents of TNF-α and IL-6 and the CaM mRNA expression were significantly decreased, while the expression of ERK mRNA was significantly increased in group IP and SP （ P 〈 0.05）. There was no significant difference in the each index metioned above between group IP and SP （ P 〉 0.05 ）. Conclusion Sevoflurane preconditioning and ischemic preconditioning can protect the lung from I/R injury through down-regulating the expression of CaM and up-regulating the expression of ERK. Key words: Anesthetics, inhalation;  Ischemic preconditioning;  Extracellular signal-regulated MAP kinases;  Calcium-calmodulin-dependent protein kinases;  Reperfusion injury;  Lung