Lizarraga I, Alfaro M J, Goicoechea C, López F, Martín M I
Departamento de Farmacología, Facultad de Medicina, Universidad Complutense de Madrid, Spain.
Neurosci Lett. 1998 Apr 24;246(2):105-8. doi: 10.1016/s0304-3940(98)00249-3.
2,3-Butanedione monoxime (BDM) has demonstrated protective effects on isolated cardiac tissues, and on smooth muscle but its mechanism of action is not fully understood. To simultaneously study the effect of BDM on muscle contractility and on neuronal activity, the effect of BDM was tested in the contractile force of myenteric plexus-longitudinal muscle strips and in electrophysiological activity of myenteric S-type neurones of guinea pig ileum. BDM reduces, in a dose-dependent manner, the force of the spontaneous motility and the contractions induced by acetylcholine, bethanechol and electrical stimulation. The same BDM concentrations depolarize the neuronal membrane and reduce the rate of evoked firing. The effect of BDM can be attributed to a direct effect on the smooth muscle and to modifications of the neuronal activity.
2,3-丁二酮一肟（BDM）已被证明对离体心脏组织和平滑肌具有保护作用，但其作用机制尚未完全明确。为了同时研究BDM对肌肉收缩性和神经元活性的影响，我们检测了BDM对豚鼠回肠肌间神经丛-纵行肌条收缩力以及肌间S型神经元电生理活性的作用。BDM以剂量依赖性方式降低自发运动的力量以及由乙酰胆碱、氨甲酰甲胆碱和电刺激诱导的收缩。相同浓度的BDM使神经元膜去极化并降低诱发放电率。BDM的作用可归因于对平滑肌的直接作用以及对神经元活性的改变。
