Department of Gastroenterology, Infectious Diseases and Rheumatology, Charité, Berlin, Germany.
Acta Physiol (Oxf). 2010 Jul 1;199(3):305-16. doi: 10.1111/j.1748-1716.2010.02096.x. Epub 2010 Feb 5.
Intestinal pressure differences or experimental distension induce ion secretion via the enteric nervous system, the sensorial origin of which is only poorly understood. This study aimed to investigate sensorial inputs and the role of afferent and interneurones in mechanically activated submucosal secretory reflex circuits.
Distension-induced rheogenic chloride secretion was measured as increase in short-circuit current 10 min after distension (DeltaI(SC)(10); distension parameters +/- 100 microL, 2 Hz, 20 s) in partially stripped rat distal colon in the Ussing-chamber in vitro. PGE(2) and PGI(2) were measured by radioimmunoassay.
DeltaI(SC)(10) was 2.0 +/- 0.2 micromol h(-1) cm(-2) and could be attenuated by lobeline, mecamylamine and dimethylphenylpiperazine, indicating an influence of nicotinergic interneurones. Additionally, a contribution of afferent neurones was indicated from the short-term potentiation of DeltaI(SC)(10) by capsaicin (1 microm). As evidence for its initial event, indomethacin (1 microm) inhibited distension-induced secretion and the release of PGI(2) was directly detected after distension. Furthermore, serotoninergic mediation was confirmed by granisetron (100 microm) which was functionally localized distally to PGI(2) in this reflex circuit, as granisetron inhibited an iloprost-induced I(SC), while indomethacin did not affect serotonin-activated ion secretion.
Distension-induced active electrogenic chloride secretion in rat colon is mediated by a neuronal reflex circuit which includes afferent neurones and nicotinergic interneurones. It is initiated by distension-induced PGI(2) release from subepithelial cells triggering this reflex via serotoninergic 5-HT(3) receptor transmission. Functionally, this mechanism may help to protect against intestinal stasis but could also contribute to luminal fluid loss, e.g. during intestinal obstruction.
肠道压力差异或实验性扩张通过肠神经系统诱导离子分泌，而肠神经系统的感觉起源知之甚少。本研究旨在探讨机械激活黏膜下分泌反射回路中的感觉传入以及传入神经元和中间神经元的作用。
在离体 Ussing 室中，通过测量部分剥离的大鼠远端结肠在 10 分钟后（DeltaI(SC)(10)；扩张参数 +/- 100 微升，2 Hz，20 秒）短电路电流的增加来测量扩张诱导的致动性氯分泌。通过放射免疫测定法测量 PGE(2)和 PGI(2)。
DeltaI(SC)(10)为 2.0 +/- 0.2 micromol h(-1) cm(-2)，可被洛贝林、美卡拉明和二甲苯哌嗪减弱，表明烟碱能中间神经元的影响。此外，辣椒素（1 微摩尔）的短期增强表明传入神经元的贡献。作为其初始事件的证据，吲哚美辛（1 微摩尔）抑制扩张诱导的分泌，并且在扩张后直接检测到 PGI(2)的释放。此外，通过格兰司琼（100 微摩尔）证实了 5-HT(3)受体介导的血清素能介导，格兰司琼在该反射回路中功能上定位于 PGI(2)的远端，因为格兰司琼抑制了伊洛前列素诱导的 I(SC)，而吲哚美辛不影响血清素激活的离子分泌。
大鼠结肠扩张诱导的主动电致氯分泌是由包括传入神经元和烟碱能中间神经元的神经元反射回路介导的。它是由上皮下细胞扩张诱导的 PGI(2)释放引发的，通过 5-HT(3)受体传递触发这种反射。从功能上讲，这种机制有助于防止肠道停滞，但也可能导致腔内液体流失，例如在肠梗阻期间。
