胆囊托基宁对suncus murinus中小肠机动性的作用
Naho Yokota1, Shota Takemi1, Ichiro Sakata2
1Area of Regulatory Biology, Division of Life Science, Graduate School of Science and Engineering, Saitama University, 255 Shimo-ohkubo, Sakuraku, Saitama 338-8570, Japan.
General and comparative endocrinology
|July 30, 2023
概括
外源胆囊托基宁 (CCK) 通过CCK1受体刺激小肠收缩. 然而,内源性CCK似乎没有参与在迁移运动复合体的第二阶段观察到的强烈的,来自小肠的收缩.
科学领域:
- 胃肠病学 胃肠病学
- 身体生理学 身体生理学
- 药理学 药理学是指药理学的学科.
背景情况:
- 禁食的胃肠道表现出三阶段的迁移运动复合体 (MMC).
- 第三阶段的MMC包括从胃扩散到下肠的收缩.
- 第二阶段小肠发作的收缩机制尚不清楚.
研究的目的:
- 研究胆囊托基宁 (CCK) 在小肠机动性中的作用.
- 为了确定CCK是否调解小肠产生的收缩.
主要方法:
- 在禁食的Suncus murinus中使用硫酸CCK-8和胃素.
- 使用龙龙胺,一个CCK1受体对抗剂.
- 在MMC的不同阶段观察运动模式.
主要成果:
- 外源性CCK-8诱导了小肠中的类似II期的收缩,被lorglumide阻断.
- 胃肠诱导胃收缩,但不是小肠收缩.
- 在II期期间,内源性CCK似乎没有调解来自小肠的强度收缩.
结论:
- 外源性CCK通过CCK1受体刺激小肠收缩.
- 内源性CCK与MMC的II阶段观察到的强烈的小肠发作的收缩无关.
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