Muallem R, Reimer R, Odes H S, Schwenk M, Beil W, Sewing K F
Gastroenterology Institute, Soroka Medical Center, Beer Sheva, Israel.
Dig Dis Sci. 1994 May;39(5):1078-84. doi: 10.1007/BF02087561.
The role of carbonic anhydrase in the process of proximal duodenal mucosal bicarbonate secretion was investigated in the guinea pig. In a series of experiments in vivo, the duodenum was perfused with 24 mmol/liter NaHCO3 solution (+ NaCl for isotonicity) to ensure that active duodenal HCO3- secretion against a concentration gradient was measured. Acetazolamide (80 mg/kg) was infused intravenously to examine the role of carbonic anhydrase on basal and agonist-stimulated HCO3- secretion. Acetazolamide abolished basal HCO3- secretion and significantly decreased HCO3- secretion after stimulation with dibutyryl 5'-cyclic adenosine monophosphate (dBcAMP, 10(-5) mol/kg), dibutyryl 5'-cyclic guanosine monophosphate (dBcGMP, 10(-5) mol/kg), prostaglandin E2 (PGE2, 10(-6) mol/kg), PGF2 alpha (10(-6) mol/kg), tetradecanoyl-phorbol-acetate (TPA, 10(-7) mol/kg), glucagon (10(-7) mol/kg), vasoactive intestinal polypeptide (VIP, 10(-8) mol/kg), and carbachol (10(-8) mol/kg). Utilizing a fluorescence technique, we could detect the enzyme carbonic anhydrase in equal amounts in villous and crypt cells of the proximal duodenal epithelium; no activity was demonstrated in tissues pretreated with acetazolamide. In conclusion, carbonic anhydrase is required for both basal and stimulated duodenal HCO3- secretion.
在豚鼠中研究了碳酸酐酶在十二指肠近端黏膜碳酸氢盐分泌过程中的作用。在一系列体内实验中，用24 mmol/L的NaHCO₃溶液（加NaCl以保持等渗）灌注十二指肠，以确保测量到十二指肠主动分泌的HCO₃⁻逆浓度梯度的情况。静脉注射乙酰唑胺（80 mg/kg），以研究碳酸酐酶对基础状态及激动剂刺激的HCO₃⁻分泌的作用。乙酰唑胺消除了基础状态下的HCO₃⁻分泌，并显著降低了用二丁酰5'-环磷酸腺苷（dBcAMP，10⁻⁵ mol/kg）、二丁酰5'-环磷酸鸟苷（dBcGMP，10⁻⁵ mol/kg）、前列腺素E₂（PGE₂，10⁻⁶ mol/kg）、前列腺素F₂α（10⁻⁶ mol/kg）、十四酰佛波醇乙酸酯（TPA，10⁻⁷ mol/kg）、胰高血糖素（10⁻⁷ mol/kg）、血管活性肠肽（VIP，10⁻⁸ mol/kg）和卡巴胆碱（10⁻⁸ mol/kg）刺激后的HCO₃⁻分泌。利用荧光技术，我们能够在十二指肠近端上皮的绒毛细胞和隐窝细胞中检测到等量的碳酸酐酶；在用乙酰唑胺预处理的组织中未显示出活性。总之，基础状态及刺激后的十二指肠HCO₃⁻分泌均需要碳酸酐酶。
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