Wali F A, Suer A H
Eur J Anaesthesiol. 1987 Jan;4(1):45-53.
The effect of atracurium on the phenomenon of post-tetanic potentiation, which is believed to be of a presynaptic origin, i.e. due to endogenous transmitter release, was investigated to see if atracurium had a presynaptic inhibitory mechanism at the rat neuromuscular junction. The results showed that atracurium (0.8-80 microM) reduced the indirectly elicited twitch, tetanic and post-tetanic twitch tensions, in a dose-dependent manner. Atracurium (1 microM) produced a tetanic fade in the preparations stimulated at 20 Hz and above. The acetylcholine (ACh) released at high frequencies of nerve stimulation was collected, in the presence of physostigmine (0.77 microM), added to a rat ileum preparation, in which it produced a small contraction which was blocked by atracurium (1 microM), which in turn blocked the contracture produced by ACh (1 microM) added directly to the organ bath. It was concluded that, in addition to its well-known competitive blockade of postsynaptic ACh receptors, atracurium may also have a presynaptic inhibitory effect at the neuromuscular junction.
阿曲库铵对强直后增强现象的影响进行了研究,强直后增强现象被认为起源于突触前,即由于内源性递质释放,以此观察阿曲库铵在大鼠神经肌肉接头处是否具有突触前抑制机制。结果表明,阿曲库铵(0.8 - 80微摩尔)以剂量依赖方式降低间接诱发的抽搐、强直和强直后抽搐张力。阿曲库铵(1微摩尔)在20赫兹及以上频率刺激的标本中产生强直衰减。在毒扁豆碱(0.77微摩尔)存在的情况下,收集高频神经刺激时释放的乙酰胆碱(ACh),添加到大鼠回肠标本中,它在其中产生小的收缩,该收缩被阿曲库铵(1微摩尔)阻断,而阿曲库铵又阻断直接添加到器官浴中的ACh(1微摩尔)产生的挛缩。得出的结论是,除了其众所周知的对突触后ACh受体的竞争性阻断作用外,阿曲库铵在神经肌肉接头处可能还具有突触前抑制作用。