权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Expression of Na channel after total colectomy in remnant ileal epithelium.

全结肠切除术后残余回肠上皮中Na通道的表达。

基本信息

批准号：
07457266
负责人：
SASAKI Iwao
金额：
$ 4.8万
依托单位：
Tohoku University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
1995
资助国家：
日本
起止时间：
1995 至 1997
项目状态：
已结题

项目摘要

Background & Aims : It has been known that in patients with proctocolectomy, epithelial transport functions in the remnant small intestine can be regulated in response to the increased fecal electrolyte and fluid loss. By using rat colectomy model, we investigated the Na and K transport mechanisms underlying the intestinal response. Methods : Proctolectomy with ileo-anal anastomosis was performed on Spregue-Dawley rats. Short-circuit current and 22Na fluxes were measured in isolated intestinal segment. Expression of mRNA for epithelial Na channels in the intestine was determined by Northern-blot analysis. Results : Amiloride (100micromol/L,mocosal side) and an amiloride analog benzamil (10micromol/L,mocosal side) reduced short-circuit current and 22Na absorption in the terminal ileum in proctocolectomized rats, but not in control rats. The activities of amirolide-sensitive short-circuit current expanded to a more proximal part (still within the ileum) between 2 and 4 wk after proctocolectomy. Plasma level of aldosterone was markedly elevated and the elevated fecal Na concentration was remarkably reduced during this period. Expression of mRNA for alpha-, beta-and gamma-subunit of epithelial Na channels in the lower small intestine was low in control, but was remarkably elevated in proctocolectomized rats. The short-circuit current, which is inhibited by tetraehyl anmonium (2 mmol/L,mucosal side), was also activated in the ileum of the colectomized rats specially in close association with the amiloride-sensitive short-circuit current. Conclusions : The electrogenic Na absorption and probably also tetraethyl ammonium-sensitive electrogenic K secretions are induced in the lower small intestine after proctocolectomy. These induction is caused by the increase of all three types of subunits, alpha-, beta- andgamma-rENaC mRNA at the transcription level. These processes may contribute to the recovery from the increased fecal Na loss.

背景与目的：已知在直结肠切除术患者中，残存小肠上皮运输功能可因粪便电解质和液体流失增加而受到调节。通过大鼠结肠切除模型，我们研究了Na和K在肠道反应中的转运机制。方法：采用Spregue-Dawley大鼠行直结肠切除术并回肠肛管吻合术。测定离体肠段的短路电流和22Na通量。Northern-blot检测肠上皮Na通道mRNA的表达。结果：阿米洛利（100微mol/L，mocosal侧）和阿米洛利类似物苯甲胺（10微mol/L，mocosal侧）降低了直结肠切除大鼠回肠末端的短路电流和22Na吸收，而对照组无此作用。在直结肠切除术后2 - 4周，氨基环素敏感短路电流的活动扩展到更近端（仍在回肠内）。血浆醛固酮水平在此期间显著升高，而粪便钠浓度在此期间显著降低。下小肠上皮Na通道α -、β -和γ -亚基mRNA的表达在对照组中较低，但在去直结肠大鼠中显著升高。四乙基铵（2 mmol/L，粘膜侧）抑制的短路电流在集束大鼠回肠中也被激活，特别是与酰胺敏感的短路电流密切相关。结论：直结肠切除术后，下小肠可诱导电致钠吸收，并可能诱导四乙基铵敏感的电致钾分泌。这些诱导是由α -、β -和γ - renac mRNA这三种亚基在转录水平上的增加引起的。这些过程可能有助于从增加的粪便钠损失中恢复。