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慢性尿毒症大鼠液体和固体标记物的胃排空及肠道转运

Gastric emptying and intestinal transit of liquid and solid markers in rats with chronic uremia.

作者信息

Wang S C, Lu K Y, Chen S M, Young T K

机构信息

Institute of Physiology, School of Life Science, National Yang-Ming University, Taipei, Taiwan, ROC.

出版信息

Chin J Physiol. 2001 Jun 30;44(2):81-7.

PMID:11530948
Abstract

Gastrointestinal motor abnormalities may account for dyspeptic symptoms of chronic uremia patients. However, the data on gastric emptying are conflicting in human studies. We, therefore, assessed gastric emptying and gastrointestinal transit in a rat uremia model. Chronic uremia was induced by five-sixths nephrectomy in the rats. After 20-hour fasting, the rats were loaded with 70 glass beads as solid markers through a gastric catheter. Two hours later, the stomach was exposed and the small intestine was equally divided into 10 segments. The glass beads in the stomach and in each intestinal segment were counted. The gastric emptying was expressed as the ratio of the number of glass beads in the small intestine to that counted from the entire gastrointestinal tract. The intestinal transit was assessed by analyzing the geometric center of the distribution of glass beads in the intestinal segments. Two conventional nonabsorbable markers, radioactive chromate and charcoal, were also used to evaluate gastric emptying and intestinal transit in the fasted state. Additionally, similar experiments of glass beads were performed in the fed state. It was found that, in the fasted state, the gastric emptying and the intestinal transit of liquid or solid markers were little affected by uremia. In the fed state, however, chronic uremia significantly decreased the intestinal transit but hardly affected the gastric emptying. We conclude that the postprandial intestinal transit, but not the gastric emptying, of solid markers may be decreased in the fed state by chronic uremia in a severity-dependent manner of a rat model, which resembles the findings in uremic patients.

摘要

胃肠道运动异常可能是慢性尿毒症患者消化不良症状的原因。然而,人体研究中关于胃排空的数据存在矛盾。因此,我们在大鼠尿毒症模型中评估了胃排空和胃肠传输。通过切除大鼠六分之五的肾脏诱导慢性尿毒症。禁食20小时后,通过胃导管给大鼠灌入70颗玻璃珠作为固体标记物。两小时后,暴露胃并将小肠等分为10段。计算胃和各肠段中的玻璃珠数量。胃排空以小肠中玻璃珠数量与整个胃肠道中玻璃珠数量之比表示。通过分析肠段中玻璃珠分布的几何中心评估肠道传输。还使用两种传统的不可吸收标记物,放射性铬酸盐和木炭,来评估禁食状态下的胃排空和肠道传输。此外,在进食状态下进行了类似的玻璃珠实验。结果发现,在禁食状态下,尿毒症对液体或固体标记物的胃排空和肠道传输影响很小。然而,在进食状态下,慢性尿毒症显著降低了肠道传输,但对胃排空影响不大。我们得出结论,在进食状态下,慢性尿毒症可能以大鼠模型中与尿毒症患者相似的严重程度依赖性方式降低固体标记物的餐后肠道传输,但不影响胃排空。

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