2-(4-苯基哌啶基)环己醇（AH5183）阻断作用的研究

Studies on the blocking action of 2-(4-phenyl piperidino) cyclohexanol (AH5183).

作者信息

Marshall I G

出版信息

Br J Pharmacol. 1970 May;38(3):503-16. doi: 10.1111/j.1476-5381.1970.tb10592.x.

DOI:10.1111/j.1476-5381.1970.tb10592.x

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1702576/

Abstract

AH5183 (2-(4-phenyl piperidino) cyclohexanol) produced neuromuscular block of slow onset in rapidly stimulated nerve-skeletal muscle preparations of the rat, chicken and cat.2. The neuromuscular block was not antagonized by neostigmine, tetraethylammonium (TEA) or choline. The rate of onset of transmission failure was enhanced by factors which increase the release of acetylcholine.3. It was concluded that the neuromuscular blocking activity was primarily pre-junctional in origin, being due either to a non-competitive action on the choline transport mechanism, or to an intracellular action on acetylcholine metabolism.4. In high doses AH5183 possessed local anaesthetic activity, but this was considered insufficient to bring about the failure of neuromuscular transmission.5. AH5183 also produced a block of sympathetically innervated preparations that was indistinguishable from that produced by an alpha-adrenoceptor blocking drug.

摘要

AH5183（2-（4-苯基哌啶基）环己醇）在大鼠、鸡和猫的快速刺激神经-骨骼肌标本中产生起效缓慢的神经肌肉阻滞。
新斯的明、四乙铵（TEA）或胆碱不能拮抗这种神经肌肉阻滞。增加乙酰胆碱释放的因素可加快传递失败的起效速率。
得出的结论是，神经肌肉阻滞活性主要源于接头前，要么是对胆碱转运机制的非竞争性作用，要么是对乙酰胆碱代谢的细胞内作用。
高剂量时，AH5183具有局部麻醉活性，但认为这不足以导致神经肌肉传递失败。
AH5183还可使交感神经支配的标本产生阻滞，这与α-肾上腺素受体阻断药产生的阻滞无法区分。