Fig. 7. Isoflurane postconditioning improved cardiac function in wild-type (WT) hearts but not in endothelial nitric oxide synthase  knockout (eNOS  −/−) hearts subjected to 30 min of global ischemia followed by 30 min of reperfusion. (A ) L eft ventricular developed pressure (LVDP) in WT hearts; (B ) LVDP in eNOS  −/−hearts; (C ) +dP/dt (maximum rate of increase of LVDP) in WT hearts; (D ) +dP/dt in eNOS  −/−hearts; (E )−dP/dt (maximum rate of decrease of LVDP) in WT hearts; (F )−dP/dt in eNOS  −/−hearts. ISO1.0= 1.0 minimum alveolar concentration of isoflurane; REP30= 30 min after reperfusion. *P < 0.05 versus  sham; # P < 0.05 versus  control (n = 10/group).

Fig. 7. Isoflurane postconditioning improved cardiac function in wild-type (WT) hearts but not in endothelial nitric oxide synthase  knockout (eNOS  −/−) hearts subjected to 30 min of global ischemia followed by 30 min of reperfusion. (A ) L eft ventricular developed pressure (LVDP) in WT hearts; (B ) LVDP in eNOS  −/−hearts; (C ) +dP/dt (maximum rate of increase of LVDP) in WT hearts; (D ) +dP/dt in eNOS  −/−hearts; (E )−dP/dt (maximum rate of decrease of LVDP) in WT hearts; (F )−dP/dt in eNOS  −/−hearts. ISO1.0= 1.0 minimum alveolar concentration of isoflurane; REP30= 30 min after reperfusion. *P < 0.05 versus  sham; # P < 0.05 versus  control (n = 10/group).

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