CAJ | 학술논문

目的探讨地氟醚对大鼠顶叶皮层神经元延迟整流钾电流(Ik)的影响.方法采用酶消化法急性分离Wistar大鼠顶叶皮层神经元,接种于培养皿,采用随机数字表法,将培养皿随机分为3组(n=10),不同浓度地氟醚组(D1～3组),在培养皿中加入含0.3 mmol/L(D1组)、0.6 mmol/L(D2组)、0.9 mmol/L(D3组)地氟醚的细胞外液灌流液.于地氟醚给药前、给药后1 min时采用全细胞膜片钳技术,记录顶叶皮层神经元Ik,计算Ik抑制率,绘制0.6 mmol/L地氟醚作用下顶叶皮层神经元Ik的电流.电压曲线、激活曲线和失活曲线.结果与给药前比较,各组给药后顶叶皮层神经元Ik降低(P＜0.01);地氟醚对顶叶皮层神经元Ik的抑制作用呈浓度依赖性(P＜0.01);0.6 mmol/L地氟醚给药后顶叶皮层神经元Ik的电流-电压曲线下移,但曲线形状和阈电位没有改变;与给药前比较,0.6mmol/L地氟醚给药后Ik的激活和失活曲线的半数激活电压和曲线斜率因子差异无统计学意义(P＞0.05).结论地氟醚对大鼠顶叶皮层神经元延迟整流钾通道具有抑制作用,且呈浓度依赖性,而对其激活和失活速率无影响,提示地氟醚对延迟整流钾通道的抑制作用并不是通过改变该通道的兴奋性而实现的,可能与其他原因有关.
목적 탐토지불미대대서정협피층신경원연지정류갑전류(Ik)적영향.방법채용매소화법급성분리Wistar대서정협피층신경원,접충우배양명,채용수궤수자표법,장배양명수궤분위3조(n=10),불동농도지불미조(D1～3조),재배양명중가입함0.3 mmol/L(D1조)、0.6 mmol/L(D2조)、0.9 mmol/L(D3조)지불미적세포외액관류액.우지불미급약전、급약후1 min시채용전세포막편겸기술,기록정협피층신경원Ik,계산Ik억제솔,회제0.6 mmol/L지불미작용하정협피층신경원Ik적전류.전압곡선、격활곡선화실활곡선.결과 여급약전비교,각조급약후정협피층신경원Ik강저(P＜0.01);지불미대정협피층신경원Ik적억제작용정농도의뢰성(P＜0.01);0.6 mmol/L지불미급약후정협피층신경원Ik적전류-전압곡선하이,단곡선형상화역전위몰유개변;여급약전비교,0.6mmol/L지불미급약후Ik적격활화실활곡선적반수격활전압화곡선사솔인자차이무통계학의의(P＞0.05).결론 지불미대대서정협피층신경원연지정류갑통도구유억제작용,차정농도의뢰성,이대기격활화실활속솔무영향,제시지불미대연지정류갑통도적억제작용병불시통과개변해통도적흥강성이실현적,가능여기타원인유관.
Objective To investigate the effects of desflurane on the delayed rectifier potassium current (Ik ) in acutely dissociated rat parietal cortical neurons. Methods Wistar rats between 10- and 14-day old of both sexes were used. The parietal cortical neurons were acutely dissociated enzymatically. The extracellular fluid saturated with 0.3,0.6 and 0.9 mmol/L desflurane was added to the culture dish, then the effects of different concentrations of desflurane on Ik were investigated by using the whole-cell patch-clamp technique in acutely dissociated rat parietal cortical neurons. Results IK was inhibited by desflurane in a concentration-dependent manner ( P ＜0.01). The V1/2 of the activation and inactivation curves and the slop factor had no change after giving 0.6 mmol/L desflurane (P ＞ 0.05). Conclusion Desflurane inhibits delayed rectifier potassium channels of parietal cortical neurons of rats in a concentration-dependent manner, and has no effect on the activation and inactivation of delayed rectifier potassium channels, indicating that the change in the excitability of the channel is not involved in the mechanism of inhibitory effect of desflurane, and the other reasons may be involved in the mechanism.