Fig. 1.
Effects of isoflurane on Na+ channel current–voltage (I-V) relations and activation. Chinese hamster ovary cells expressing various rat Na+ channel α-subunit isoforms were subjected to whole cell patch clamp recording. Voltage of peak INa activation (Vmax) was 0 mV for Nav1.2 (A), −10 mV for Nav1.4 (B), and −30 mV for Nav1.5 (C). Isoflurane (0.8 mm, approximately 2.2 times minimum alveolar concentration28) inhibited all three isoforms. Data were fitted to a Boltzmann equation yielding voltage of 50% maximal activation (V1/2a) and slope factor (k) values. Isoflurane had no effect on V1/2a. Protocol: 100-ms prepulse from a holding potential of −100 mV, 25-ms test potential from −60 to +80 mV in 10-mV increments, pulses applied at 5-s intervals. Mean isoflurane concentrations were 0.82 ± 0.06 mm for Nav1.2, 0.78 ± 0.06 mm for Nav1.4, and 0.81 ± 0.05 mm for Nav1.5 (mean ± SEM, n = 4–7).

Effects of isoflurane on Na+ channel current–voltage (I-V) relations and activation. Chinese hamster ovary cells expressing various rat Na+ channel α-subunit isoforms were subjected to whole cell patch clamp recording. Voltage of peak INa activation (Vmax) was 0 mV for Nav1.2 (A), −10 mV for Nav1.4 (B), and −30 mV for Nav1.5 (C). Isoflurane (0.8 mm, approximately 2.2 times minimum alveolar concentration28) inhibited all three isoforms. Data were fitted to a Boltzmann equation yielding voltage of 50% maximal activation (V1/2a) and slope factor (k) values. Isoflurane had no effect on V1/2a. Protocol: 100-ms prepulse from a holding potential of −100 mV, 25-ms test potential from −60 to +80 mV in 10-mV increments, pulses applied at 5-s intervals. Mean isoflurane concentrations were 0.82 ± 0.06 mm for Nav1.2, 0.78 ± 0.06 mm for Nav1.4, and 0.81 ± 0.05 mm for Nav1.5 (mean ± SEM, n = 4–7).

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