Fozard J R, Muscholl E
Br J Pharmacol. 1974 Apr;50(4):531-41. doi: 10.1111/j.1476-5381.1974.tb08586.x.
1 The effects of 4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethylammonium chloride (McN-A-343) and N-benzyl-3-pyrrolidyl acetate methobromide (AHR 602) on cardiac performance and noradrenaline release from terminal sympathetic fibres were measured in isolated perfused hearts of rabbits.2 In the presence of sufficient atropine to block muscarinic receptors, high concentrations of McN-A-343 and AHR 602 caused no cardiac stimulation and there was no increase in the resting output of noradrenaline into the perfusates.3 McN-A-343 and AHR 602 increased both the mechanical responses and the transmitter overflow evoked by electrical stimulation of the sympathetic nerves (SNS) but inhibited both parameters during perfusion with 1,1-dimethyl-4-phenylpiperazinium (DMPP). The effects were atropine-resistant and qualitatively similar to those seen with cocaine. Hexamethonium inhibited DMPP, but affected neither SNS per se nor the facilitatory effects of McN-A-343 and AHR 602 on SNS.4 McN-A-343, cocaine and desipramine (but not AHR 602 or hexamethonium) blocked the net cardiac noradrenaline uptake and increased the positive chronotropic effect of noradrenaline.5 Prior perfusion with concentrations of cocaine and desipramine sufficient to block uptake reduced or abolished the facilitatory effects of both McN-A-343 and AHR 602 on SNS.6 Cocaine, McN-A-343 and AHR 602 displayed local anaesthetic properties on the guinea-pig wheal and frog nerve plexus tests, and their relative potencies in this respect were similar to those for inhibition of DMPP-evoked transmitter overflow. Hexamethonium did not produce local anaesthesia.7 The results indicate that the facilitated release of noradrenaline after SNS and the inhibition of release after DMPP produced by McN-A-343 and AHR 602 are the result of their combined local anaesthetic action and inhibition of amine uptake.
在兔离体灌流心脏中，测定了4-（间氯苯基氨甲酰氧基）-2-丁炔基三甲基氯化铵（McN-A-343）和N-苄基-3-吡咯烷基乙酸甲基溴（AHR 602）对心脏功能以及交感神经末梢纤维去甲肾上腺素释放的影响。
在存在足以阻断毒蕈碱受体的阿托品时，高浓度的McN-A-343和AHR 602不会引起心脏兴奋，且灌注液中去甲肾上腺素的静息输出量也没有增加。
McN-A-343和AHR 602增加了交感神经（SNS）电刺激所诱发的机械反应和递质溢出，但在用1,1-二甲基-4-苯基哌嗪鎓（DMPP）灌注期间抑制了这两个参数。这些作用对阿托品有抗性，且在性质上与可卡因所见的作用相似。六甲铵抑制DMPP，但既不影响SNS本身，也不影响McN-A-343和AHR 602对SNS的促进作用。
McN-A-343、可卡因和地昔帕明（但不是AHR 602或六甲铵）阻断了心脏对去甲肾上腺素的净摄取，并增强了去甲肾上腺素的正性变时作用。
预先用足以阻断摄取的可卡因和地昔帕明浓度进行灌注，可降低或消除McN-A-343和AHR 602对SNS的促进作用。
可卡因、McN-A-343和AHR 602在豚鼠风团和蛙神经丛试验中表现出局部麻醉特性，它们在这方面的相对效力与抑制DMPP诱发的递质溢出的效力相似。六甲铵不会产生局部麻醉作用。
结果表明，McN-A-343和AHR 602在SNS后促进去甲肾上腺素释放以及在DMPP后抑制释放是它们联合的局部麻醉作用和胺摄取抑制作用的结果。
