From the capacitance study of the oleylamine planar lipid bilayer, a model is proposed in which the interaction of anesthetics and bilayers occurs in two mechanisms: anesthetics adsorb on the bilayer/water interface at low anesthetic concentrations near the clinical level, saturate the interface as the concentrations increase, and then penetrate into the hydrophobic core at concentrations above the surface saturation. The present study measured the electrical conductance of the oleylamine bilayer. In the absence of anesthetics, the conductance was 3.2 × 10 −8 S·cm −2 at 293.15°K. In the low anesthetic concentration range below the point where the capacitance reached a limiting value of 0.58 μF·cm −2 ( A b, the conductance was little affected the anesthetics. When the anesthetic concentration exceeded the critical point, the conductance suddenly increased sharply. The conductance increase was analyzed by considering the following three factors: (1) ionized oleylamine molecules, (2) anesthetic molecules adsorbed on the bilayer surface, and (3) anesthetic molecules solvated into the bilayer core. In the absence of anesthetics, the theoretical value for the energy required for the Cl − ion to penetrate into the bilayer was estimated to be 1.56 × 10 5 J·mol −1 when an ion pair is not formed, and 8.07 × 10 4 J·mol −1 when an ion pair is formed with the ionized oleylamine molecule. At anesthetic concentrations lower than the critical point, decrease of relative permittivity at the interface by anesthetic molecules assists the penetration of Cl − ion into the bilayer core. When anesthetics molecules are adsorbed on the bilayer surface at saturation, the value was estimated to be 7.46 × 10 4 J·mol −1. At supraclinical anesthetic concentrations above the surface saturation level, the presence of anesthetic molecules in the bilayer core further decreased the value to 7.043 × 10 4 J·mol −1 at maximum anesthetic concentration, above which the bilayer was destabilized (capacitance = 0.67 μF·cm −2). This is apparently caused by the increase in relative permittivity in the bilayer core. The dependency of the bilayer conductance on pH and anesthetic concentrations can be explained by the interfacial adsorption of inhalation anesthetics decreasing the relative permittivity of the interfacial region at clinical concentrations. The present result supports the two-process model prosed in the accompanying paper for the interaction of anesthetics with membranes.