Hellström P M
Acta Physiol Scand. 1986 Sep;128(1):47-55. doi: 10.1111/j.1748-1716.1986.tb07948.x.
Neurotensin has previously been shown to delay gastric emptying, gastrointestinal transit and ileo-caecal emptying in the rat. To investigate the vagal influence on these effects of neurotensin, separate groups of rats were operated with combined vagotomy and pyloroplasty or with pyloroplasty alone and compared to a group of normal rats. All animals were supplied with a permanent gastrointestinal catheter and a venous catheter. After operation the rats were allowed to recover for 7 days, and were fasted for 24 h prior to the experiments. A radioactive marker of 1.0-0.5 ml Na2(51)CrO4 in isotonic polyethylene glycol 400 was instilled intraluminally in the stomach, proximal or distal the small intestine. Saline (control animals) or neurotensin (test animals) was given i.v. in each group studied. The animals were killed at 15, 30, 60, and 120 min after administration of the marker. The distribution of the marker in the gastrointestinal tract was registered with a scintillation detector and quantitative analysis of the amount of radioactivity retained in separate gastrointestinal segments was carried out. Gastric emptying was delayed by combined vagotomy and pyloroplasty (P less than 0.01) compared to pyloroplasty alone and normals. Neurotensin at doses of 6 (P less than 0.05) and 12 (P less than 0.01) pmol kg-1 min-1 retarded gastric emptying dose-dependently in normals and rats with pyloroplasty alone, but did not further slow the gastric emptying in rats with vagotomy and pyloroplasty. However, at a dose of 24 pmol kg-1 min-1 neurotensin delayed gastric emptying (P less than 0.01) compared to controls. Gastrointestinal transit was slowed down by neurotensin at a dose of 6 pmol kg-1 min-1 in normals (P less than 0.01) and rats with pyloroplasty alone (P less than 0.05). In rats with vagotomy and pyloroplasty, neurotensin at doses of 6 and 12 pmol kg-1 min-1 had no effect on gastrointestinal transit.(ABSTRACT TRUNCATED AT 250 WORDS)
神经降压素此前已被证明可延缓大鼠的胃排空、胃肠传输及回盲部排空。为研究迷走神经对神经降压素这些作用的影响,将大鼠分成不同组,分别进行迷走神经切断术与幽门成形术联合手术或仅进行幽门成形术,并与一组正常大鼠作比较。所有动物均植入永久性胃肠导管和静脉导管。术后让大鼠恢复7天,实验前禁食24小时。将1.0 - 0.5 ml含放射性标记的Na2(51)CrO4等渗聚乙二醇400经腔内注入胃、小肠近端或远端。在每组研究对象中,静脉注射生理盐水(对照动物)或神经降压素(实验动物)。给药后15、30、60和120分钟处死动物。用闪烁探测器记录标记物在胃肠道的分布,并对各胃肠道节段留存的放射性量进行定量分析。与仅行幽门成形术及正常大鼠相比,迷走神经切断术与幽门成形术联合手术使胃排空延迟(P < 0.01)。剂量为6(P < 0.05)和12(P < 0.01)pmol kg-1 min-1的神经降压素在正常大鼠和仅行幽门成形术的大鼠中剂量依赖性地延缓胃排空,但在迷走神经切断术与幽门成形术联合手术的大鼠中并未进一步减慢胃排空。然而,与对照组相比,剂量为24 pmol kg-1 min-1的神经降压素使胃排空延迟(P < 0.01)。剂量为6 pmol kg-1 min-1的神经降压素使正常大鼠(P < 0.01)和仅行幽门成形术的大鼠(P < 0.05)的胃肠传输减慢。在迷走神经切断术与幽门成形术联合手术的大鼠中,剂量为6和12 pmol kg-1 min-1的神经降压素对胃肠传输无影响。(摘要截于250字)