乙酰唑胺抑制人近端十二指肠的基础和刺激状态下的HCO₃⁻分泌。

Acetazolamide inhibits basal and stimulated HCO3- secretion in the human proximal duodenum.

作者信息

Knutson T W, Koss M A, Hogan D L, Isenberg J I, Knutson L

机构信息

Division of Gastroenterology, University of California at San Diego.

出版信息

Gastroenterology. 1995 Jan;108(1):102-7. doi: 10.1016/0016-5085(95)90013-6.

DOI:10.1016/0016-5085(95)90013-6

PMID:7806030

Abstract

BACKGROUND/AIMS: Carbonic anhydrase activity plays a role in electrolyte transport in many tissues. This study examined the effect of the carbonic anhydrase inhibitor acetazolamide on human basal and prostaglandin E2- and acid-stimulated duodenal mucosal bicarbonate secretion and transmucosal electrical potential difference.

METHODS

Seven healthy volunteers participated in four separate experiments. The variables included oral acetazolamide vs. control test and, as agonists of bicarbonate secretion, either luminal acidification or luminal prostaglandin E2. The proximal 4 cm of the duodenum (i.e., the duodenal bulb) was isolated between balloons as previously described and perfused with an HCO(3-)-containing (24 mmol/L) balanced electrolyte glucose-containing (10 mmol/L) solution.

RESULTS

Acetazolamide treatment significantly decreased mean basal HCO3- secretion and basal transmucosal potential difference. After luminal acidification, duodenal mucosal bicarbonate increased significantly after both acetazolamide treatment (mean, 626; 95% CI, 91-1160 mumol.cm-1.h-1) and in the control tests (mean, 868; 95% CI, 652-1084 mumol.cm-1.h-1). However, acetazolamide treatment significantly decreased prostaglandin E2-stimulated HCO3- secretion from 461 (95% CI, 307-615) to 222 (95% CI, 121-324) mumol.cm-1.h-1.

CONCLUSIONS

Duodenal mucosal carbonic anhydrase activity has an important function in the regulation of basal and prostaglandin E2-stimulated human duodenal mucosal bicarbonate transport.

摘要

背景/目的：碳酸酐酶活性在许多组织的电解质转运中发挥作用。本研究考察了碳酸酐酶抑制剂乙酰唑胺对人十二指肠黏膜基础碳酸氢盐分泌以及前列腺素E2和酸刺激的碳酸氢盐分泌和跨黏膜电位差的影响。

方法

7名健康志愿者参与了4个独立实验。变量包括口服乙酰唑胺与对照试验，以及作为碳酸氢盐分泌激动剂的管腔酸化或管腔前列腺素E2。如前所述，将十二指肠近端4厘米（即十二指肠球部）用球囊隔开，并灌注含HCO(3-)（24 mmol/L）的平衡电解质葡萄糖溶液（10 mmol/L）。

结果

乙酰唑胺治疗显著降低了平均基础HCO3-分泌和基础跨黏膜电位差。管腔酸化后，乙酰唑胺治疗组（平均值为626；95%可信区间为91 - 1160 μmol·cm-1·h-1）和对照试验组（平均值为868；95%可信区间为652 - 1084 μmol·cm-1·h-1）的十二指肠黏膜碳酸氢盐均显著增加。然而，乙酰唑胺治疗显著降低了前列腺素E2刺激的HCO3-分泌，从461（95%可信区间为307 - 615）降至222（95%可信区间为121 - 324）μmol·cm-1·h-1。