American Society of Anesthesiologists

Figure 6. The effect of sevoflurane on voltage-sensitive Calcium2+ current (ICa) evoked from isolated guinea pig ventricular myocytes at room temperature. The dotted lines indicate the zero transmembrane current level. Control (open circle); 0.7 mM sevoflurane (closed circle). (A) From a holding potential of -80 mV, a test potential to -40 mV evoked a low-threshold, T-type Calcium2+ current (ICa,T). (B) High-threshold ICa, ICa,L, triggered by a voltage step to 0 mV from a holding potential of -80 mV. (C) Normalization of the ICa,L after anesthetic administration to the control peak ICa,L clearly shows that sevoflurane causes a increase in the apparent rate of inactivation. (D) Effect of sevoflurane on steady-state inactivation of I sub Ca,L. Myocytes were held at a prepulse voltage ranging from -110 mV to +5 mV for 5 s before triggering a test pulse to 0 mV to measure peak ICa,L. Currents were not corrected for leak and capacitive artifact; instead leakage current was considered negligible at 0 mV. For each myocyte, the peak inward current evoked from each prepulse voltage was normalized to the peak ICa,L and fitted to the Boltzmann function with parameters describing the voltage for half steady-state inactivation, Vn, and the slope factor, kn. For control steady-state inactivation (open circle); Vn= -27 mV and kn= -5.6 mV; after exposure to 0.7 mM sevoflurane (closed circle): Vn= -34 mV and kn= -5.1 mV.

Figure 6. The effect of sevoflurane on voltage-sensitive Calcium²+ current (I^Ca) evoked from isolated guinea pig ventricular myocytes at room temperature. The dotted lines indicate the zero transmembrane current level. Control (open circle); 0.7 mM sevoflurane (closed circle). (A) From a holding potential of -80 mV, a test potential to -40 mV evoked a low-threshold, T-type Calcium²+ current (I^Ca,T). (B) High-threshold I^Ca, I^Ca,L, triggered by a voltage step to 0 mV from a holding potential of -80 mV. (C) Normalization of the I^Ca,L after anesthetic administration to the control peak I^Ca,L clearly shows that sevoflurane causes a increase in the apparent rate of inactivation. (D) Effect of sevoflurane on steady-state inactivation of I sub Ca,L. Myocytes were held at a prepulse voltage ranging from -110 mV to +5 mV for 5 s before triggering a test pulse to 0 mV to measure peak I^Ca,L. Currents were not corrected for leak and capacitive artifact; instead leakage current was considered negligible at 0 mV. For each myocyte, the peak inward current evoked from each prepulse voltage was normalized to the peak I^Ca,L and fitted to the Boltzmann function with parameters describing the voltage for half steady-state inactivation, Vⁿ, and the slope factor, kⁿ. For control steady-state inactivation (open circle); Vⁿ= -27 mV and kⁿ= -5.6 mV; after exposure to 0.7 mM sevoflurane (closed circle): Vⁿ= -34 mV and kⁿ= -5.1 mV.

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