Effects of serotonin on rat ileocolonic transit and fluid transfer in vivo: possible mechanisms of action.
Effects of serotonin on rat ileocolonic transit and fluid transfer in vivo: possible mechanisms of action.
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DOI：
10.1136/gut.34.6.794
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发表时间：
1993-06
期刊：
影响因子：
24.5
通讯作者：
L. Oosterbosch;M. R. Ohe;Miguel A. Valdovinos;L. Kost;Sidney F. Phillips;Michael Camilleri
中科院分区：
文献类型：
--
作者：
L. Oosterbosch;M. R. Ohe;Miguel A. Valdovinos;L. Kost;Sidney F. Phillips;Michael Camilleri
目的：探讨5-羟色胺（5-HT）对回结肠连接部（ICJ）功能的影响。在麻醉大鼠中，建立模型以研究主动脉内（IA）5-羟色胺对回结肠和结肠转运的影响，以及对许多5 HT受体拮抗剂转运的影响。在第一系列的实验中，用99 mTc DTPA标记的盐水团被滴注到ICJ近端20 cm处，并且在3小时后通过同位素扩散的几何中心来评估转运。在第二个系列中，在盲肠后结肠上使用了类似的技术，并在两小时后进行了运输评估。在第三系列实验中，通过在大鼠血浆样电解质溶液中使用14 C聚乙二醇（PEG）4000作为不可吸收标记物的标准灌注实验来评价ia 5 HT对回肠净流体通量的影响。与生理盐水相比，5-HT显著加速ICJ的传输（p < 0.05）。这种加速作用可与氨甲酰甲胆碱的作用相媲美。腹腔注射阿托品、5-HT受体拮抗剂麦角新碱、酮色林、扎考必利和5-HT-4激动剂SC 53116可抑制5-HT对ICJ转运的影响。甲麦角胺、扎考必利和SC 53116与ia 5 HT联合给药使ICJ通过速率减慢至低于单独ia生理盐水的速率。当这些相同的药物与生理盐水一起给药时，ICJ通过没有显著改变。在加速ICJ转运的剂量下，5-羟色胺没有显著改变结肠转运或回肠液体转运。总之，5 HT是一种有效的药理刺激过境大鼠ICJ在体内，5 HT的作用是介导的部分通过毒蕈碱神经元和几个5 HT受体亚型。
The aim was to investigate the action of serotonin (5HT) on function of the ileocolonic junction (ICJ) in vivo. In anaesthetised rats, models were developed to study the effects of intra-aortic (ia) serotonin on ileocolonic and colonic transit, and the effects on transit of a number of 5HT receptor antagonists. In the first series of experiments, a bolus of saline labelled with 99mTc DTPA was instilled 20 cm proximal to the ICJ and transit was assessed three hours later by the geometric centre of the spread of isotope. In the second series, similar techniques were used on the postcaecal colon and transit assessed two hours later. In the third series of experiments, the effects of ia 5HT on ileal net fluid flux was evaluated by standard perfusion experiments with 14C polyethylene glycol (PEG) 4000 as a non-absorbable marker in rat plasma-like electrolyte solution. Compared with ia saline, 5HT accelerated ICJ transit significantly (p < 0.05). This acceleration was comparable with the effect of ia bethanechol. The effects of 5HT on ICJ transit were inhibited by the intraperitoneal (ip) infusion of atropine, the 5HT receptor antagonists, methysergide, ketanserin, zacopride, and the 5HT4 agonist, SC53116. Methysergide, zacopride, and SC53116 given with ia 5HT slowed ICJ transit to rates below those of ia saline alone. When these same agents were given together with ia saline, the ICJ transit was not significantly altered. Serotonin, at the dose that accelerated ICJ transit, did not significantly alter colonic transit or ileal fluid transport. In conclusion, 5HT is a potent pharmacological stimulant of transit across the rat ICJ in vivo; the action of 5HT is mediated partly through muscarinic neurones and several 5HT receptor subtypes.