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...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.展开更多
Background：Calcium regulatory proteins-L-type Ca^2＋ channels （LTCCs）,ryanodine receptor 2 （RyR2）,and Na^＋/Ca^2＋ exchanger isoform 1 （NCX1） have been recognized as important protective mechanisms during myoca...Background：Calcium regulatory proteins-L-type Ca^2＋ channels （LTCCs）,ryanodine receptor 2 （RyR2）,and Na^＋/Ca^2＋ exchanger isoform 1 （NCX1） have been recognized as important protective mechanisms during myocardial ischemia-reperfusion injury （I/RI）.Both sevofturane postconditioning （SevoPoC） and delayed remote ischemic preconditioning （DRIPC） have been shown to protect the heart against I/RI.In this study,we aimed to compare the effects of SevoPoC and DRIPC on the expression of the three calcium regulatory proteins in an isolated rat heart model.Methods：After 30-min balanced perfusion,isolated hearts from rats were subjected to 30-min ischemia followed by 60-min reperfusion.Totally 40 isolated hearts were randomly assigned to four groups （n =10/group）：time control group,I/RI group,SevoPoC group,and DRIPC group.The effect of SevoPoC （3% v/v） and DRIPC were observed.Myocardial infarct size （IS）,cardiac troponin I level,and heart function were measured.The protein and messenger RNA levels of LTCCs,RyR2,and NCX1 were determined.Results：Both SevoPoC and DRIPC improved the recovery of myocardial function,and reduced cardiac troponin Ⅰ release after I/RI.The decrease in IS was more significant in the SevoPoC group than that in the DRIPC group （16.50% ± 4.54% in the SevoPoC group [P =0.0006],and 22.34% ± 4.02% in the DRIPC group [P =0.0007] vs.35.00% ± 5.24% in the I/RI group,respectively）.SevoPoC,but not DRIPC significantly inhibited the activity of NCX 1 （0.59 ＋ 0.09 in the I/RI group vs.0.32 ± 0.16 in the SevoPoC group,P =0.006;vs.0.57 ± 0.14 in the DRIPC group,P =0.072）.No statistical significant differences were observed in the expression of LTCCs and RyR2 between SevoPoC and DRIPC.In addition,subsequent correlation analysis showed a significantly positive relationship between the cardiac troponin Ⅰ level and the protein expression ofNCX1 （r =0.505,P =0.023）.Conclusion：SevoPoC may be more effective in the cardioprotection than DRIPC partly due to the deactivation of NCX1.展开更多
文摘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.
文摘Background：Calcium regulatory proteins-L-type Ca^2＋ channels （LTCCs）,ryanodine receptor 2 （RyR2）,and Na^＋/Ca^2＋ exchanger isoform 1 （NCX1） have been recognized as important protective mechanisms during myocardial ischemia-reperfusion injury （I/RI）.Both sevofturane postconditioning （SevoPoC） and delayed remote ischemic preconditioning （DRIPC） have been shown to protect the heart against I/RI.In this study,we aimed to compare the effects of SevoPoC and DRIPC on the expression of the three calcium regulatory proteins in an isolated rat heart model.Methods：After 30-min balanced perfusion,isolated hearts from rats were subjected to 30-min ischemia followed by 60-min reperfusion.Totally 40 isolated hearts were randomly assigned to four groups （n =10/group）：time control group,I/RI group,SevoPoC group,and DRIPC group.The effect of SevoPoC （3% v/v） and DRIPC were observed.Myocardial infarct size （IS）,cardiac troponin I level,and heart function were measured.The protein and messenger RNA levels of LTCCs,RyR2,and NCX1 were determined.Results：Both SevoPoC and DRIPC improved the recovery of myocardial function,and reduced cardiac troponin Ⅰ release after I/RI.The decrease in IS was more significant in the SevoPoC group than that in the DRIPC group （16.50% ± 4.54% in the SevoPoC group [P =0.0006],and 22.34% ± 4.02% in the DRIPC group [P =0.0007] vs.35.00% ± 5.24% in the I/RI group,respectively）.SevoPoC,but not DRIPC significantly inhibited the activity of NCX 1 （0.59 ＋ 0.09 in the I/RI group vs.0.32 ± 0.16 in the SevoPoC group,P =0.006;vs.0.57 ± 0.14 in the DRIPC group,P =0.072）.No statistical significant differences were observed in the expression of LTCCs and RyR2 between SevoPoC and DRIPC.In addition,subsequent correlation analysis showed a significantly positive relationship between the cardiac troponin Ⅰ level and the protein expression ofNCX1 （r =0.505,P =0.023）.Conclusion：SevoPoC may be more effective in the cardioprotection than DRIPC partly due to the deactivation of NCX1.
