IMPAIRED PROXIMAL DUODENAL MUCOSAL BICARBONATE SECRETION IN PATIENTS WITH DUODENAL-ULCER
IMPAIRED PROXIMAL DUODENAL MUCOSAL BICARBONATE SECRETION IN PATIENTS WITH DUODENAL-ULCER
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DOI：
10.1056/nejm198702123160704
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发表时间：
1987-02-12
影响因子：
158.5
通讯作者：
KOSS, MA
中科院分区：
文献类型：
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作者：
ISENBERG, JI;SELLING, JA;KOSS, MA
防止人十二指肠粘膜酸性和消化性损伤的防御因素还没有得到充分的评估。为了确定静止期十二指肠溃疡患者十二指肠粘膜碳酸氢盐的产生是否发生改变，我们测定了健康人和静止期十二指肠溃疡患者十二指肠球部和十二指肠远端的基础碳酸氢盐和酸刺激的碳酸氢盐的排出量。与16名正常受试者相比，12名患者十二指肠近端粘膜碳酸氢盐基础分泌量(+-SE)显著减少(185。+-)。13对107。+-。每小时每厘米18微克分子；P<；0.001)。此外，对直接向十二指肠球部注入生理性剂量的盐酸(每5分钟2 mmol)，患者十二指肠近端碳酸氢盐的最大排出量是正常反应(263±-)的41%。65比642。+-。每小时每厘米77微克分子；P<；0.01)。不同群体之间几乎没有重叠。相比之下，两组十二指肠远端的碳酸氢盐排出量相似。我们的结论是，大多数十二指肠溃疡患者在静息状态下十二指肠近端粘膜碳酸氢盐的产生减少，对盐酸的反应与胃酸分泌高峰有关。十二指肠近端粘膜碳酸氢盐分泌受损可能是十二指肠溃疡发生和自然发展的重要因素。
The defensive factors that prevent the human duodenal mucosa from acidic and peptic damage have not been fully evaluated. To determine whether duodenal mucosal bicarbonate production was altered in patients with inactive duodenal ulcer, we measured basal and acid-stimulated bicarbonate output from the duodenal bulb and the distal duodenum in healthy subjects and patients with inactive duodenal ulcer. As compared with 16 normal subjects, the 12 patients had significantly less mean (.+-.SE) basal proximal duodenal mucosal bicarbonate secretion (185 .+-. 13 vs. 107 .+-. 18 .mu.mol per centimeter per hour; P < 0.001). Moreover, in response to a physiologic amount of hydrochloric acid (2 mmol per five minutes) instilled directly into the duodenal bulb, peak proximal duodenal bicarbonate output in the patients was 41 percent of the normal response (263 .+-. 65 vs. 642 .+-. 77 .mu.mol per centimeter per hour; P < 0.01). There was little overlap between groups. In contrast, bicarbonate outputs in the distal duodenum were similar in the two groups. We conclude that most patients with duodenal ulcer disease have decreased proximal duodenal mucosal bicarbonate production at rest, in response to hydrochloric acid, and in relation to peak gastric acid secretion. Impaired proximal duodenal mucosal bicarbonate secretion may be an important factor in the development and natural history of duodenal ulcer.