Impaired gastrocolonic response and peristaltic reflex in slow-transit constipation:: role of 5-HT3 pathways

Impaired gastrocolonic response and peristaltic reflex in slow-transit constipation:: role of 5-HT3 pathways
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DOI:
10.1152/ajpgi.00082.2001
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发表时间:
2002-08-01
影响因子:
4.5
通讯作者:
Hasler, WL
Hasler, WL
中科院分区:
医学2区
文献类型:
--
作者:
Björnsson, ES;Chey, WD;Hasler, WL

文献摘要

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结肠运动由 5-羟色胺 (5-HT)(3) 依赖性胃结肠反应和 5-HT3 独立蠕动反射调节。我们比较了 13 名健康志愿者和 9 名慢传输性便秘患者双盲安慰剂或格拉司琼后降结肠张力对胃窦扩张、十二指肠脂质灌注和结肠扩张的反应。胃窦扩张(100-300 ml)和十二指肠脂质(3 kcal/min)会引起志愿者结肠张力的增加,而便秘患者的结肠张力则减弱(P < 0.05)。格拉司琼 (10 μg/kg) 降低了志愿者对胃窦扩张和脂质的反应以及便秘患者对脂质的反应 (P < 0.05)。便秘患者蠕动反射的上升收缩减弱(P < 0.05),而下降反应相似。格拉司琼不会改变蠕动反射。患者和志愿者的结肠对氨甲酰甲胆碱的反应相似。总之,胃窦扩张和十二指肠脂质激活的胃结肠反应和蠕动反射的上升收缩因慢传输型便秘而受损,同时丧失 5-HT3 依赖性和非依赖性功能。因此,结肠运动功能的神经反射调节异常可能在慢传输性便秘中发挥病理生理作用。
Colonic motility is modulated by the 5-hydroxytryptamine (5-HT)(3)-dependent gastrocolonic response and 5-HT3-independent peristaltic reflex. We compared descending colon tone responses to antral distension, duodenal lipid perfusion, and colonic distension after double-blind placebo or granisetron in 13 healthy volunteers and nine slow-transit constipated patients. Antral distension (100-300 ml) and duodenal lipids (3 kcal/min) evoked increases in colon tone in volunteers, which were blunted in constipated patients (P < 0.05). Granisetron (10 μg/kg) reduced responses to antral distension and lipids in volunteers and to lipids in constipated patients (P < 0.05). The ascending contraction of the peristaltic reflex was blunted in constipated patients (P < 0.05), whereas descending responses were similar. Granisetron did not modify the peristaltic reflex. Colonic responses to bethanechol were similar in patients and volunteers. In conclusion, antral distension- and duodenal lipid-activated gastrocolonic responses and ascending contractions of the peristaltic reflex are impaired with slow-transit constipation with loss of both 5-HT3-dependent and -independent function. Thus abnormalities of neural reflex modulation of colonic motor function may play pathophysiological roles in slow-transit constipation.