Moser H, Heinemeyer D, Asal M, Schlue W R
Institut für Zoologie I, Universität Düsseldorf, Federal Republic of Germany.
Pflugers Arch. 1988 Oct;412(6):589-96. doi: 10.1007/BF00583759.
The experiments were performed with double-barelled micro-electrodes in Retzius neurones of the leech in order to see if the tertiary amine local anesthetic procaine affects intracellular pH (pHi) and its regulation. Lasting about 20 min, exposures to procaine (3 mM) saline caused an intracellular alkalosis of about 0.2 pH units which gradually degradated; its removal initiated a fast decrease of pHi resulting in an acidosis, fron which the cells recovered. Detailed studies, involving CO2 or NH4+ acid loaded cells as well as inhibition of the pHi regulating exchange mechanism by various drugs or exposures to Na-free salines suggest, that neither the Na+ -H+, nor a probably Na+ -dependent HCO3-(-)Cl- exchange are affected by procaine. We propose a model for procaine action on pHi assuming that neutral procaine passes the membrane easily through lipophilic pathways. The degradation of alkalinity during procaine exposure hints on an entry of loaded procaine, some possible transport paths of which are discussed.
实验采用双管微电极在水蛭的Retzius神经元中进行,以观察叔胺类局部麻醉药普鲁卡因是否会影响细胞内pH值(pHi)及其调节。暴露于含3 mM普鲁卡因的盐溶液中约20分钟,会导致细胞内碱化约0.2个pH单位,且这种碱化会逐渐消退;去除普鲁卡因后,pHi会迅速下降导致酸中毒,随后细胞恢复。详细研究涉及用CO2或NH4+使细胞酸化,以及用各种药物抑制pHi调节交换机制或暴露于无钠盐溶液中,结果表明,普鲁卡因既不影响Na+-H+交换,也不影响可能依赖Na+的HCO3-(-)Cl-交换。我们提出了一个普鲁卡因对pHi作用的模型,假设中性普鲁卡因通过亲脂性途径容易穿过细胞膜。普鲁卡因暴露期间碱度的消退提示了带电荷的普鲁卡因的进入,文中讨论了其一些可能的运输途径。