Fig. 3. Activation of sarcolemmal adenosine triphosphate-sensitive potassium channel during oxidative stress, but not during isoflurane pretreatment, is essential for the protective effects of isoflurane preconditioning. (  A ) Protection by isoflurane (APC  vs . stress) was abolished in the presence of HMR-1098 (APC + HMR), whereas blockade of sarcolemmal adenosine triphosphate-sensitive potassium channel had no effect on cell damage by oxidative stress (stress + HMR) or cell death in time control (TC + HMR). *  P < 0.05  versus stress, stress + HMR, and APC + HMR. All values were significantly different  versus TC + HMR group. (  B ) Isoflurane-induced protection (APC  vs . stress) was abolished when HMR-1098 was applied during the stress period (APC + HMRstress), but not during isoflurane pretreatment (APC + HMRISO). *  P < 0.05  versus stress and APC + HMRstress. 

Fig. 3. Activation of sarcolemmal adenosine triphosphate-sensitive potassium channel during oxidative stress, but not during isoflurane pretreatment, is essential for the protective effects of isoflurane preconditioning. (  A ) Protection by isoflurane (APC  vs . stress) was abolished in the presence of HMR-1098 (APC + HMR), whereas blockade of sarcolemmal adenosine triphosphate-sensitive potassium channel had no effect on cell damage by oxidative stress (stress + HMR) or cell death in time control (TC + HMR). *  P < 0.05  versus stress, stress + HMR, and APC + HMR. All values were significantly different  versus TC + HMR group. (  B ) Isoflurane-induced protection (APC  vs . stress) was abolished when HMR-1098 was applied during the stress period (APC + HMRstress), but not during isoflurane pretreatment (APC + HMRISO). *  P < 0.05  versus stress and APC + HMRstress. 

Close Modal

or Create an Account

Close Modal
Close Modal