Di Croce D E, Trinks P W, de La Cal C, Sánchez G A, Takara D
Biophysics Department, School of Dentistry, University of Buenos Aires, M T de Alvear 2142, 17th floor B, Buenos Aires, 1122AAH, Argentina.
Naunyn Schmiedebergs Arch Pharmacol. 2014 Sep;387(9):873-81. doi: 10.1007/s00210-014-1004-2. Epub 2014 Jun 20.
Myotoxic effects related to intracellular Ca(2+) disturbances have been reported for local anesthetics. Such effects might derive from Ca-ATPase dysfunction. The aim of this work was to describe the effect of lidocaine and bupivacaine on the sarcoplasmic reticulum (SR) Ca-ATPase from fast-twitch skeletal muscle and to identify the affected steps of the enzyme's cycle. SR sealed vesicles were isolated from rabbit fast-twitch muscles by ultracentrifugation. The effect of the anesthetics on Ca-ATPase activity was assessed with a colorimetric method and Ca(2+) binding, uptake, phosphorylation of the enzyme by ATP, Ca(2+) dissociation kinetics and phosphoenzyme formation and decomposition levels were tested with radioisotopic methods. Lidocaine and bupivacaine inhibited Ca-ATPase activity with half-maximal inhibitory concentrations (Ki) of 25.3 and 31.4 mM, respectively, and the steady-state Ca(2+) transport ability with Ki values of 33.6 and 46.5 mM, decreasing the maximal transport rate without modification of the Ca(2+) or ATP affinity for the enzyme. This is consistent with an absence of competition for the transport and catalytic sites. The anesthetics did not inhibit Ca(2+) binding but inhibited the phosphorylation partial reactions. Ca(2+) dissociation kinetics was not affected, but the phosphoenzyme levels were decreased, and the decomposition rate of the phosphoenzyme became faster in the presence of the anesthetics. It is concluded that lidocaine and bupivacaine at concentrations available in pharmaceutical formulations for clinical medical and dental uses inhibit the SR Ca-ATPase through inhibition of key phosphorylation steps of the enzymatic cycle.
局部麻醉药的肌毒性作用与细胞内钙离子紊乱有关。这种作用可能源于钙 -ATP酶功能障碍。本研究的目的是描述利多卡因和布比卡因对快肌骨骼肌肌浆网(SR)钙 -ATP酶的影响,并确定该酶循环中受影响的步骤。通过超速离心从兔快肌中分离出SR封闭囊泡。用比色法评估麻醉药对钙 -ATP酶活性的影响,并用放射性同位素方法检测钙离子结合、摄取、ATP对酶的磷酸化作用、钙离子解离动力学以及磷酸化酶的形成和分解水平。利多卡因和布比卡因抑制钙 -ATP酶活性,其半数最大抑制浓度(Ki)分别为25.3和31.4 mM,抑制稳态钙离子转运能力的Ki值分别为33.6和46.5 mM,降低了最大转运速率,而未改变钙离子或ATP对该酶的亲和力。这与对转运和催化位点不存在竞争一致。麻醉药不抑制钙离子结合,但抑制磷酸化部分反应。钙离子解离动力学不受影响,但磷酸化酶水平降低,并且在有麻醉药存在时磷酸化酶的分解速率加快。得出结论,临床医疗和牙科用药制剂中可用浓度的利多卡因和布比卡因通过抑制酶循环的关键磷酸化步骤来抑制SR钙 -ATP酶。