Fig. 2.
Concentration-dependent protective effect of sevoflurane against H2O2-induced hypercontracture. (A), Percentage of hypercontracted myocytes measured at 5, 10, and 15 min after exposure to H2O2 (100 μm) in the absence and presence of sevoflurane (SEVO) at various concentrations (0.5, 1, 2, 3, and 5%). ** P < 0.01 compared with control at each superfusion time. †† P < 0.01 compared with 0 min in control group, § P < 0.05 and §§ P < 0.01 compared with 0 min in SEVO 0.5% group, ‡ P < 0.01 compared with 0 min in SEVO 1% group. (B) Concentration-dependent prevention of H2O2-induced hypercontracture by sevoflurane, measured at 15 min of exposure to H2O2 (100 μm). The data points were fitted with a Hill equation:  where R is the percentage of hypercontracted myocytes, R0 is the percentage of hypercontracted myocytes without SEVO, [SEVO] is the millimolar concentration of SEVO, IC50 is the concentration of SEVO causing a half-maximal response, and nH is Hill coefficient. The smooth curve through the data points represents a least-squares fit, yielding an IC50 of 0.194 mm and nH of 2.0. The millimolar concentration of SEVO has a linear correlation with the volume percentage (0.5–5%) of SEVO delivered via the vaporizer as follows; (SEVO; in mm) = 0.14592 × (SEVO; in %) − 0.0025182. ** P < 0.01 compared with control. The data shown were obtained from multiple experiments of confocal imaging of fluo-3 fluorescence in ventricular myocytes (N = 3–4) at room temperature (23°–25°C).

Concentration-dependent protective effect of sevoflurane against H2O2-induced hypercontracture. (A), Percentage of hypercontracted myocytes measured at 5, 10, and 15 min after exposure to H2O2 (100 μm) in the absence and presence of sevoflurane (SEVO) at various concentrations (0.5, 1, 2, 3, and 5%). ** P < 0.01 compared with control at each superfusion time. †† P < 0.01 compared with 0 min in control group, § P < 0.05 and §§ P < 0.01 compared with 0 min in SEVO 0.5% group, ‡ P < 0.01 compared with 0 min in SEVO 1% group. (B) Concentration-dependent prevention of H2O2-induced hypercontracture by sevoflurane, measured at 15 min of exposure to H2O2 (100 μm). The data points were fitted with a Hill equation: where R is the percentage of hypercontracted myocytes, R0 is the percentage of hypercontracted myocytes without SEVO, [SEVO] is the millimolar concentration of SEVO, IC50 is the concentration of SEVO causing a half-maximal response, and nH is Hill coefficient. The smooth curve through the data points represents a least-squares fit, yielding an IC50 of 0.194 mm and nH of 2.0. The millimolar concentration of SEVO has a linear correlation with the volume percentage (0.5–5%) of SEVO delivered via the vaporizer as follows; (SEVO; in mm) = 0.14592 × (SEVO; in %) − 0.0025182. ** P < 0.01 compared with control. The data shown were obtained from multiple experiments of confocal imaging of fluo-3 fluorescence in ventricular myocytes (N = 3–4) at room temperature (23°–25°C).

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