CAJ | 학술논문

目的评价氯胺酮对大鼠颈上交感神经节神经元烟碱诱发电流的影响.方法采用胰酶消化法急性分离新生Wistar大鼠颈上交感神经节神经元,接种于培养皿,培养5～7d后采用膜片钳全细胞模式测定烟碱诱发电流,记录50 μmol/L烟碱和与不同浓度(10、25、50、100 μmol/L)氯胺酮混合溶液作用下烟碱诱发的峰电流及受体失敏时间常数,计算其抑制烟碱诱发电流的半数有效浓度.结果 10、25、50和100 μmol/L氯胺酮呈浓度依赖性地抑制烟碱诱发的峰电流(P＜0.05).与50 μmol/L烟碱诱发电流相比,氯胺酮50、100 μmol/L给药后受体快失敏相和慢失敏相时间常数均缩短(P＜0.05).氯胺酮对烟碱诱发电流的抑制作用符合指数方程,其抑制烟碱诱发电流的半数有效浓度＜20μmol/L.结论氯胺酮可呈浓度依赖性地抑制大鼠颈上交感神经节神经元烟碱诱发电流,提示氯胺酮对交感神经节神经元活动具有抑制作用,可能是其在某些特定情况下降低血压的机制之一.
목적 평개록알동대대서경상교감신경절신경원연감유발전류적영향.방법 채용이매소화법급성분리신생Wistar대서경상교감신경절신경원,접충우배양명,배양5～7d후채용막편겸전세포모식측정연감유발전류,기록50 μmol/L연감화여불동농도(10、25、50、100 μmol/L)록알동혼합용액작용하연감유발적봉전류급수체실민시간상수,계산기억제연감유발전류적반수유효농도.결과 10、25、50화100 μmol/L록알동정농도의뢰성지억제연감유발적봉전류(P＜0.05).여50 μmol/L연감유발전류상비,록알동50、100 μmol/L급약후수체쾌실민상화만실민상시간상수균축단(P＜0.05).록알동대연감유발전류적억제작용부합지수방정,기억제연감유발전류적반수유효농도＜20μmol/L.결론 록알동가정농도의뢰성지억제대서경상교감신경절신경원연감유발전류,제시록알동대교감신경절신경원활동구유억제작용,가능시기재모사특정정황하강저혈압적궤제지일.
Objective To investigate the effect of ketamine on nicotine-induced current in rat superior cervical ganglion neurons.Methods Newborn Wistar rats were used in this study.Neurons were isolated enzymatically from superior cervical ganglia of newborn rats in an aseptic condition and cultured in 90％ DMEM/F12,10％ horse serum containing penicillin 100 μg/ml for 5-7 d.Nicotine-induced current was measured and recorded using whole-cell patch clamp technique.A mixture of nicotine 50 μmol/L and different concentrations of ketamine ( 10,25,50,100 μmol/L) was added to the isolated neurons.The effect of ketamine on nicotine-induced current was evaluated.Results Nicotine-induced peak current was inhibited by ketamine in a concentration-dependent manner.The time constant of fast and slow desensitizing phase of the nicotine acetylcholine receptor was shortened after being exposed to the mixture of nicotine 50 μmol/L + 50 or 100 μmol/L ketamine as compared to nicotine 50 μmol/L-induced current.The median effective concentration of ketamine inhibiting nicotine-induced current was less than 20 μmol/L.Conclusion Ketamine can decrease nicotine-induced current in rat superior cervical ganglion neurons in a concentration-dependent manner indicating that inhibition of sympathetic activity is involved in the mechanism of decrease in BP by ketamine in specific condition.