Urazaev A K, Naumenko N V, Poletayev G I, Nikolsky E E, Vyskocil F
State Medical University, Kazan, Russia.
Neuroreport. 1997 Jan 20;8(2):403-6. doi: 10.1097/00001756-199701200-00004.
Muscle fibres of the rat diaphragm kept in a tissue culture medium became depolarized by 8-10 mV within 3 h after denervation. In the presence of carbachol (CB; 5 x 10(-8) M), and acetylcholine (ACh; 5 x 10(-8) M, the post-denervation depolarization was reduced. Both drugs were used in concentrations which mimicked the effect of non-quantal release of ACh. (+)Tubocurarine (TC) and ouabain did not prevent the protective action of CB, indicating that this effect is not mediated through ACh nicotinic receptors or the electrogenic Na+, K+ pump. Addition of Mg2+, verapamil, diltiazem, nifedipine and Cd2+ in concentrations which block Ca2+ entry virtually inhibited the effect of both cholinomimetics. L-Nitroarginine methylester (NAME), an inhibitor of NO synthase, and haemoglobin, an extracellular scavenger of the NO radical, completely eliminated the protective effect of CB on post-denervation depolarization. The retrograde action of NO produced by cholinomimetics on nerve terminals is postulated.
在组织培养基中培养的大鼠膈肌肌纤维在去神经支配后3小时内去极化8 - 10 mV。在存在卡巴胆碱（CB；5×10⁻⁸ M）和乙酰胆碱（ACh；5×10⁻⁸ M）的情况下，去神经支配后的去极化现象有所减轻。两种药物的使用浓度模拟了乙酰胆碱非量子释放的效果。（+）筒箭毒碱（TC）和哇巴因并未阻止CB的保护作用，表明这种作用不是通过乙酰胆碱烟碱受体或电生性钠钾泵介导的。添加能阻断钙离子内流的浓度的镁离子、维拉帕米、地尔硫䓬、硝苯地平和镉离子实际上抑制了两种拟胆碱药的作用。一氧化氮合酶抑制剂L - 硝基精氨酸甲酯（NAME）和细胞外一氧化氮自由基清除剂血红蛋白完全消除了CB对去神经支配后去极化的保护作用。推测拟胆碱药产生的一氧化氮对神经末梢具有逆行作用。
