Serotonin stimulates endotoxin translocation via 5-HT3 receptors in the rat ileum.
Serotonin stimulates endotoxin translocation via 5-HT3 receptors in the rat ileum.
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DOI：
10.1152/ajpgi.00376.2002
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发表时间：
2003-05
期刊：
影响因子：
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通讯作者：
Tadanori Yamada;A. Inui;N. Hayashi;M. Fujimura;M. Fujimiya
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文献类型：
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作者：
Tadanori Yamada;A. Inui;N. Hayashi;M. Fujimura;M. Fujimiya
由于之前很少有研究调查肠梗阻引起的内毒素易位的机制，因此我们的目的是阐明从肠嗜铬（EC）细胞释放的血清素[5-羟色胺（5-HT）]是否负责改变粘膜对内毒素的通透性，并确定介导这种作用的5-HT受体亚型。将FITC标记的LPS（FITC-LPS）注射到大鼠回肠中，随后使用荧光分光光度计测量肠系膜上静脉中的FITC-LPS水平。为了测量高腔内压力诱导的 5-HT 释放，使用了血管和腔内灌注的大鼠回肠的离体制备。结果表明，升高的腔内压力会刺激 FITC-LPS 的易位和 5-HT 从 EC 细胞释放到肠腔中，但不会进入门静脉循环。这种 FITC-LPS 易位是由管腔和颈静脉中外源施加的 5-HT 刺激的，而管腔内和静脉内施用 5-HT(3) 受体拮抗剂可抑制这种易位。管腔内和静脉内给予5-HT(3)受体拮抗剂可抑制管腔内压力升高对FITC-LPS易位的刺激作用。这些结果表明，EC 细胞释放的 5-HT 可能参与了腔内压力升高引起的 FITC-LPS 易位，并且这种效应是由可能位于肠上皮中的 5-HT(3) 受体介导的。
Because few previous studies have investigated the mechanisms of endotoxin translocation induced by intestinal obstruction, we aimed to clarify whether or not serotonin [5-hydroxytryptamine (5-HT)], which is released from enterochromaffin (EC) cells, is responsible for alterations of the mucosal permeability to endotoxin and to identify the 5-HT receptor subtypes that mediate this action. FITC-labeled LPS (FITC-LPS) was injected into the ileum of rats, and the FITC-LPS level in the superior mesenteric vein was subsequently measured by using a fluorescence spectrophotometer. To measure the 5-HT release induced by high intraluminal pressure, ex vivo preparation of vascularly and luminally perfused rat ileum was used. Results demonstrated that elevated intraluminal pressure stimulates the translocation of FITC-LPS and the release of 5-HT from the EC cells into the intestinal lumen but not into the portal circulation. This FITC-LPS translocation, which was stimulated by exogenously applied 5-HT in the lumen and the jugular vein, was inhibited by 5-HT(3) receptor antagonist administration both intaluminally and intravenously. The stimulatory effect of elevated intraluminal pressure on the translocation of FITC-LPS was inhibited by the intraluminal and intravenous administration of 5-HT(3) receptor antagonist. These results suggest that 5-HT released from EC cells may be involved in the translocation of FITC-LPS induced by elevated intraluminal pressure and that this effect is mediated by 5-HT(3) receptors that may be located in the intestinal epithelium.