Lin H C, Ueda I, Lin S H, Shieh D D, Kamaya H, Eyring H
Biochim Biophys Acta. 1980 May 8;598(1):51-65. doi: 10.1016/0005-2736(80)90265-5.
Adsorption of procaine and tetracaine to the dipalmitoyl phosphatidylcholine monolayers at the air/water interface is analyzed in terms of two types of interaction: (1) between the phospholipid molecules and the ligand molecules, and (2) among the ligand molecules themselves. The presence of the phospholipid monolayer increases the surface concentration of the anesthetics. The interaction energy, omega AB, between the phospholipid molecules and the anesthetic molecules at the interface accounts for this excess adsorption. The values were --2.95 kT for procaine and --2.99 kT for tetracaine where k is the Boltzmann constant and T = 298 K. The adsorption of the local anesthetics to the interface was cooperative. The interaction energy, omega AA, between the anesthetics molecules on the surface determines the cooperativity. The values were --0.056 kT for procaine and --0.397 kT for tetracaine, where T = 298 K. This parameter determines the slope of the curve plotted relating the surface concentration (gamma) and the logarithm of the bulk concentration (log C). When (omega AA/kT) greater than or equal to 1, the adsorption follows the phase-transition. A parameter KA, which is related to the difference of the free energy of anesthetics between the surface and the bulk molecules, locates the take-off point of the adsorption curve at the log C axis. The values were 2.15 x 10(3) for procaine and 7.00 x 10(3) for tetracaine. In spite of the general assumption that the difference in the clinical potency among local anesthetics are attributable to their lipid solubility, the present results showed that the phospholipid-anesthetic interaction energies for procaine and tetracaine were similar. The larger surface concentration of tetracaine than procaine at the same bulk concentration was due to the combined effect of KA and omega AA. KA represents the tendency of the anesthetic molecules to escape from the hydrogen-bonded water phase, and omega AA determines the cooperativity factor causing these molecules to aggregate at the interface. It was also observed that the charged forms of the anesthetics have non-zero surface activities.
通过两种相互作用来分析普鲁卡因和丁卡因在空气/水界面处对二棕榈酰磷脂酰胆碱单分子层的吸附作用：（1）磷脂分子与配体分子之间的相互作用，以及（2）配体分子自身之间的相互作用。磷脂单分子层的存在增加了麻醉剂的表面浓度。界面处磷脂分子与麻醉剂分子之间的相互作用能ωAB解释了这种过量吸附现象。对于普鲁卡因，该值为–2.95 kT，对于丁卡因，该值为–2.99 kT，其中k为玻尔兹曼常数，T = 298K。局部麻醉剂在界面处的吸附是协同的。表面上麻醉剂分子之间的相互作用能ωAA决定了协同性。对于普鲁卡因，该值为–0.056 kT，对于丁卡因，该值为–0.397 kT，其中T = 298K。该参数决定了绘制的表面浓度（γ）与本体浓度对数（log C）相关曲线的斜率。当（ωAA/kT）大于或等于1时，吸附遵循相变规律。一个与表面分子和本体分子之间麻醉剂自由能差异相关的参数KA确定了吸附曲线在log C轴上的起始点。对于普鲁卡因，该值为2.15×10³，对于丁卡因，该值为7.00×10³。尽管一般认为局部麻醉剂临床效力的差异归因于它们的脂溶性，但目前的结果表明，普鲁卡因和丁卡因的磷脂-麻醉剂相互作用能相似。在相同本体浓度下，丁卡因比普鲁卡因具有更高的表面浓度是KA和ωAA共同作用的结果。KA代表麻醉剂分子从氢键结合水相逸出的趋势，而ωAA决定了导致这些分子在界面处聚集的协同因子。还观察到麻醉剂的带电形式具有非零表面活性。
