Stein R D, Backman S B, Collier B, Polosa C
Department of Anaesthesia, Royal Victoria Hospital, Montreal, Quebec, Canada.
Can J Anaesth. 1998 Oct;45(10):1011-8. doi: 10.1007/BF03012310.
To evaluate the effect of edrophonium on synaptic transmission in the superior cervical ganglion.
In anaesthetized rats the effect of edrophonium on synaptic transmission was studied in vitro by testing whether it blocks the compound action potential recorded from postganglionic fibres evoked by stimulation of preganglionic axons. The superior cervical ganglion was excised and the cervical sympathetic trunk and internal carotid nerve were used for stimulating and recording, respectively. Drugs superfused included edrophonium (0.1-500 microM), neostigmine (0.1-10 microM), and muscarinic M1 and M2 antagonists pirenzepine and AFDX-116 (200 nM-10 microM), respectively. To evaluate a presynaptic action, the effect of edrophonium on basal and high-K+ (35 mM) evoked release of [3H]ACh from the superior cervical ganglion was studied in vitro. To evaluate a postsynaptic action, edrophonium's effect on postganglionic nerve discharge in response to arterial injection of ACh (100 micrograms) into the superior cervical ganglion was determined in vivo.
Edrophonium (10-500 microM) decreased the compound action potential amplitude (ED50 163.5 microM). A decrease was not produced by neostigmine, nor was it reversed by pirenzepine or AFDX-116. Edrophonium blocked postganglionic cell firing in response to exogenously administered ACh. Although edrophonium did not affect basal or high-K+ evoked ACh release, when the evoked increase was calculated as a multiple of the basal release, it caused approximately a 30% (P < 0.005) reduction.
Edrophonium blocks ganglionic cholinergic transmission postsynaptically and, possibly, presynaptically. The mechanism(s) by which this occurs does not appear to involve inhibition of cholinesterase, or activation of M1 or M2 receptor subtypes.
评估依酚氯铵对上颈神经节突触传递的影响。
在麻醉大鼠中，通过测试依酚氯铵是否阻断刺激节前轴突诱发的节后纤维复合动作电位，在体外研究其对突触传递的影响。切除上颈神经节，分别使用颈交感干和颈内动脉神经进行刺激和记录。灌注的药物包括依酚氯铵（0.1 - 500微摩尔）、新斯的明（0.1 - 10微摩尔）以及毒蕈碱M1和M2拮抗剂哌仑西平及AFDX - 116（分别为200纳摩尔 - 10微摩尔）。为评估突触前作用，在体外研究依酚氯铵对基础状态及高钾（35毫摩尔）诱发的上颈神经节[3H]乙酰胆碱释放的影响。为评估突触后作用，在体内确定依酚氯铵对向上颈神经节动脉注射乙酰胆碱（100微克）后节后神经放电的影响。
依酚氯铵（10 - 500微摩尔）降低复合动作电位幅度（半数有效量为163.5微摩尔）。新斯的明未产生降低作用，哌仑西平或AFDX - 116也不能使其逆转。依酚氯铵阻断对外源性给予乙酰胆碱的节后细胞放电。尽管依酚氯铵不影响基础状态或高钾诱发的乙酰胆碱释放，但当诱发增加量以基础释放量的倍数计算时，它导致约30%（P < 0.005）的降低。
依酚氯铵在突触后及可能在突触前阻断神经节胆碱能传递。发生这种情况的机制似乎不涉及胆碱酯酶抑制或M1或M2受体亚型的激活。
