Hayashi E, Shinozuka K, Maeda T, Takeda M
Eur J Pharmacol. 1983 May 6;89(3-4):229-34. doi: 10.1016/0014-2999(83)90498-3.
The study concerned the effect of ascorbate on the contractile response induced by DMPP in the guinea-pig ileal longitudinal muscle. At 0.5-10 mM, sodium ascorbate shifted the dose-response curve for DMPP to the left and enhanced the maximum contraction. On the other hand, in the presence of ascorbate, the high potassium (40 mM)-induced contraction was not altered, and the contraction by acetylcholine and histamine in concentrations higher than 1 microM and 0.3 microM, respectively, was slightly reduced. Thus, ascorbate enhanced the contractile response caused by DMPP which induced acetylcholine release from nerve terminals indirectly by stimulating the ganglia of the Auerbach's plexus elements. This potentiating effect of ascorbate was studied with a dual organ bath which was partitioned into two compartments. When the oral half of the muscle strip was directly stimulated by DMPP applied to the oral compartment, a contraction of the unstimulated anal part was observed. This contraction was blocked by atropine or adenosine applied to the unstimulated part. Tetrodotoxin, applied to the stimulated part, abolished the contraction of the unstimulated part. The contraction of the unstimulated part was enhanced by ascorbate applied to the stimulated part but not to the unstimulated part. These results indicate that the contraction observed in the unstimulated part may have been caused by acetylcholine release from cholinergic nerves as a result of conduction of the oral part excitation by DMPP along cholinergic nerve fibers; ascorbate may have affected the ganglion cells in Auerbach's plexus to potentiate the action of DMPP.
该研究关注了抗坏血酸盐对豚鼠回肠纵肌中由二甲基苯基哌嗪（DMPP）诱导的收缩反应的影响。在0.5 - 10 mM浓度下，抗坏血酸钠使DMPP的剂量 - 反应曲线向左移动，并增强了最大收缩力。另一方面，在存在抗坏血酸盐的情况下，高钾（40 mM）诱导的收缩未改变，而乙酰胆碱和组胺在分别高于1 microM和0.3 microM浓度时引起的收缩略有降低。因此，抗坏血酸盐增强了由DMPP引起的收缩反应，DMPP通过刺激奥尔巴赫神经丛的神经节间接诱导神经末梢释放乙酰胆碱。使用分隔为两个隔室的双器官浴研究了抗坏血酸盐的这种增强作用。当通过施加到口腔隔室的DMPP直接刺激肌肉条的口腔端时，观察到未刺激的肛门端出现收缩。这种收缩被施加到未刺激部分的阿托品或腺苷阻断。施加到刺激部分的河豚毒素消除了未刺激部分的收缩。施加到刺激部分而非未刺激部分的抗坏血酸盐增强了未刺激部分的收缩。这些结果表明，在未刺激部分观察到的收缩可能是由于DMPP使口腔端的兴奋沿着胆碱能神经纤维传导，导致胆碱能神经释放乙酰胆碱所致；抗坏血酸盐可能影响了奥尔巴赫神经丛中的神经节细胞，从而增强了DMPP的作用。
