Sevoflurane preconditioning and postconditioning attenuate apoptosis induced by ischemia-reperfusion in rat lung

Objective To investigate the effect of sevoflurane preconditioning and postconditioning on lung ischemia-reperfusion(IR) injury and apoptosis in rat.Methods Wistar rats were randomly assigned to four groups:sham group(n =6):no ischaemia-reperfusion;IR group(n =6):left lung ischemia was achieved by clamping the hilum for 90 min,followed by 120 min reperfusion;sev+pre group(n =6):1 minimum alveolar concentration(MAC) sevoflurane was admi-nistered for 30 min prior to ischemia;sev+post group(n =6):ischemia was followed by 1 MAC sevoflurane postconditioning at the first 30 min reperfusion.PaO2 was measured after reperfusion.The number of apoptotic cells was estimated using the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling(TUNEL) technique.Results After ischemia-reperfusion,a significant deterioration of PaO2 was noticed and the number of apoptotic cells remarkably increased compared with that of sham group.In sev+pre group and sev+post group,PaO2 was(85.7±14.4) mmHg and(88.6±12.5) mmHg respectively,which was apparently increased compared with that in IR group [(63.9±11.3) mmHg,P <0.05].The number of apoptotic cells in sev+pre group [(6.94 ± 1.49)%] and sev+post group [(7.69 ± 1.61)%] was significantly lower than that in IR group [(12.12 ± 2.77)%,P <0.05].But all parameters showed no significant difference between sev+pre group and sev+post group.Conclusions Both sevoflurane preconditioning and postconditioning could prevent lung ischemia-reperfusion injury and attenuate apoptosis in rat.

Objective To investigate the effect of sevoflurane preconditioning and postconditioning on lung ischemia-reperfusion （IR） injury and apoptosis in rat. Methods Wistar rats were randomly assigned to four groups： sham group （n =6）： no ischaemia-reperfusion; IR group （n =6）： left lung ischemia was achieved by clamping the hilum for 90 rain, followed by 120 min reperfusion; sev＋pre group （n =6）： 1 minimum alveolar concentration （MAC） sevoflurane was admi- nistered for 30 min prior to ischemia; sev＋post group （n =6）： ischemia was followed by 1 MAC sevoflurane postconditioning at the first 30 min reperfusion. PaO2 was measured after reperfusion. The number of apoptotic cells was estimated using the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling （TUNEL） technique. Results After ischemia-reperfusion, a significant deterioration of PaO2 was noticed and the number of apoptotic cells remarkably increased compared with that of sham group. In sev＋pre group and sev＋post group, PaO2 was （85.7± 14.4） mmHg and （88.6± 12.5） mmHg respectively, which was apparently in- creased compared with that in IR group [（63.9± 11.3） mmHg, P 〈0.05]. The number of apoptotic cells in sev＋pre group [（6.94 ±1.49）%] and sev＋post group [（7.69± 1.61）%] was significantly lower than that in IR group [（12.12 ± 2.77）%, P 〈0.05]. But all parameters showed no significant difference between sev＋pre group and sev＋post group. Conclusions Both sevoflurane preconditioning and postcond）t）oning could prevent lung ischemiareperfusion injury and attenuate apoptosis in rat.