Waters A, Harder D R
Neurosurgery. 1983 Dec;13(6):676-80. doi: 10.1227/00006123-198312000-00011.
Force development, intracellular membrane potential (Em), and voltage vs. current curves were measured in rat basilar artery to help elucidate the mechanism of action of morphine sulfate and a synthetic narcotic, meperidine hydrochloride, on this preparation. Morphine sulfate caused a dose-dependent contraction of these vessels, which was reversible with naloxone. Electrical studies show that morphine may act upon this vascular smooth muscle preparation by decreasing potassium conductance (gk). This hypothesis is supported by the findings that morphine sulfate depolarized these cells and increased the input resistance (rin) determined by the application of rectangular hyperpolarizing and depolarizing current pulses through the microelectrode during impalement and recording of the associated voltage changes (delta V). Meperidine hydrochloride had significantly less effect on this preparation than morphine sulfate. Further studies show that the vehicular medium used for the commercially available preparation of naloxone (viz. the methyl and propyl esters of p-hydroxybenzoic acid in a ratio of 9:1) is, in vitro, a vasodilator of cerebral vascular smooth muscle.
在大鼠基底动脉中测量了力的产生、细胞内膜电位（Em）以及电压与电流曲线，以帮助阐明硫酸吗啡和合成麻醉剂盐酸哌替啶对该制剂的作用机制。硫酸吗啡引起这些血管的剂量依赖性收缩，用纳洛酮可使其逆转。电生理学研究表明，吗啡可能通过降低钾电导（gk）作用于这种血管平滑肌制剂。这一假设得到以下发现的支持：硫酸吗啡使这些细胞去极化，并增加了输入电阻（rin），该电阻是在通过微电极施加矩形超极化和去极化电流脉冲以记录相关电压变化（δV）时测定的。盐酸哌替啶对该制剂的作用明显小于硫酸吗啡。进一步研究表明，用于市售纳洛酮制剂的载体介质（即对羟基苯甲酸甲酯和丙酯，比例为9:1）在体外是脑血管平滑肌的血管舒张剂。
