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中国临床药理学与治疗学 ›› 2009, Vol. 14 ›› Issue (12): 1366-1370.

• 基础研究 • 上一篇    下一篇

A 型肉毒毒素抑制Methoxamine和电场刺激引发主动脉肌条的收缩

宗晓健1,3, 宋焱峰1, 张雪平4, 侯一平1,2   

  1. 1兰州大学基础医学院神经科学研究所, 甘肃 730000, 兰州;
    2甘肃省新药临床前研究重点实验室, 甘肃 730000, 兰州;
    3甘肃省第二人民医院, 甘肃 730000, 兰州;
    4兰州生物制品研究所, 甘肃 730046, 兰州
  • 收稿日期:2009-04-16 修回日期:2009-10-20 发布日期:2020-10-20
  • 通讯作者: 侯一平, 男, 教授, 博士生导师, 研究方向:神经科学。E-mail:houyiping@lzu.edu.cn
  • 作者简介:宗晓健, 女, 硕士, 研究方向:神经科学。
  • 基金资助:
    兰州大学医学科研基金(LZUYX200605); 甘肃省科技支撑计划(090NKCA112); 甘肃省新药临床前重点研究实验室资助(KLPSGS0802)

Inhibitory effect of botulinum toxin type A on isolated aortic contractility-induced by Methoxamine and electric field stimulation

ZONG Xiao-jian1,3, SONG Yan-feng1, ZHANG Xue-ping4, HOU Yi-ping1,2   

  1. 1Department of Neuroscience, School of BasicMedical Sciences, Lanzhou 730000, Gansu, China;
    2Key Laboratory of Preclinical Study for New Drugs of Gansu Province, Lanzhou Univeristy, Lanzhou 730000, Gansu, China;
    3Gansu Provincial Second People's Hospital, Lanzhou 730000, Gansu, China;
    4Lanzhou Institute of Biologic Products, Lanzhou 730046, Gansu, China
  • Received:2009-04-16 Revised:2009-10-20 Published:2020-10-20

摘要: 目的:观察A 型肉毒毒素(botulinum toxin type A, BTX-A)对肾上腺素α受体激动剂Methoxamine (MOA)和电场刺激(electrical field stimulation, EFS)引发主动脉肌条收缩的作用。方法:在95 %O2 和5 %CO2 条件下, 将不同条件处理的兔腹主动脉0.5 cm ×3.0 cm 螺旋形肌条悬挂于37 ℃Krebs 液的浴槽内, 记录收缩张力变化。MOA 组:MOA 5 μmol/L 引发收缩30 min 后分别加入Krebs 液(对照, n =10)、BTX-A 50 (n =10)或100 U mL (n = 10 ), 30 min 后再加入MOA5 μmol/L 。EFS 组:EFS 50 Hz, 80 V, 1 ms, 60 s 持续性引发肌条收缩30 min 后分别加入Krebs 液(对照, n =10)或BTX-A 50 U mL (n =10), 30 min后再加入MOA 5 μmol/L 。结果:BTX-A 50 、100 U mL 分别导致MOA 诱发的肌条收缩张力下降80 %(P <0.01)和95 %(P <0.01), 再加入MOA 引发BTX-A 干预过肌条的收缩力仅为对照组的35 %(P <0.01)和3 %(P <0.01), 该抑制作用呈剂量依赖关系。BTX-A 50 U mL 导致EFS 诱发的肌条收缩张力下降94 %(P <0.01), 后续加入MOA 引发BTX-A 处理过的肌条, 收缩力下降为对照组的10 %(P <0.01)。结论:肾上腺素α受体激动剂MOA 和EFS 引发兔主动脉肌条收缩,BTX-A 抑制MOA 和EFS 引发动脉平滑肌收缩作用机理与抑制NA 的释放和其受体有关。

关键词: A 型肉毒毒素, 主动脉, 电场刺激, 去甲肾上腺素

Abstract: AIM: To observe the inhibitory effect of botulinum toxin type A (BTX-A)on rabbit aortic contractility- induced by methoxamine (MOA), an agonist of noradrenergic αreceptor, and electric field stimulation (EFS) in vitro.METHODS: MOA and EFS treated groups were carried out in this study.0.5 cm ×3.0 cm spiral-shaped strip of rabbit abdominal aorta was suspended in incubation bath containing Krebs bicarbonate buffer (pH 7.4, constant 37 ℃)with 95 % O2 and 5 %CO2, and the change of muscular force was recorded.Strips in MOA-treated group were administrated with MOA 5 μmol/L for promoting contraction for 30 min, followed by Krebs (as control, n =10), BTX-A 50 U mL (n =10)or 100 U mL (n =10)addition for 30 min recording, and subsequently treated with MOA 5 μmol/L again.Other strips in the EFS treated group were persistently stimulated by 50 Hz, 80 V, 1 ms and 60 s electricity, followed by Krebs (n = 10)or BTX-A 50 U mL (n =10)addition for 30min, and subsequently treated with MOA 5 μmol/L again. RESULTS: BTX-A given at 50 and 100 U mL was dose-dependently decreased aortic contractility-induced by MOA by 80 %(P <0.01)and 95 %(P <0.01), respectively.The contractile tension of the strips-treated with BTX-A at 50 and 100 U mL induced by MOA wer 35 %(P <0.01)and 3 %(P <0.01)respectively in comparison with control group.The aortic contractility- induced by EFS was decreased by 94 %(P < 0.01)with BTX-A 50 U mL.The contractile tension MOA repeated addition into the strips-treated with EFS +BTX-A at 50 U mL were decreased to 10 % (P < 0.01)in comparison with control group.CONCLUSION: MOA, an agonist of noradrenergic αreceptor, and EFS, can promote rabbit aortic contractility.BTXA inhibits arterial smooth muscular contractility-induced by MOA and EFS,which is related to inhibiting noradrenergic release and its receptor.

Key words: botulinum toxin type A, aorta, electrical field stimulation, noradrenaline

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