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本实验旨在探讨ＨＣＯ３－分泌的调节及其转运的离子通道。取大白兔近端十二指肠，置于尤氏小室间（ＵｓｓｉｎｇＣｈａｍｂｅｒ），测定血管活血肠肽（ＶＩＰ）、前列腺素Ｅ２（ＰＧＥ２），二丁酰环磷腺甙（ｄｂ－ｃＡＭＰ）及电刺激（ＥＦＳ）对碳酸氢盐（ＨＣＯ３－）分泌量、电流（Ｉｓｃ）和电位差（ＰＤ）的影响，以及缺氧、缺氯、缺钠和加入ＤＩＤＳ（４，４－ｄｉｉｓｏｔｈｉｏｃｙａｎｏｓｔｉｌｂｅｎｅ－２，２’－ｄｉｓｕｌｆｏｎｉｃａｃｉｄ）、哇巴因（Ｏｕａｂａｉｎ）和神经毒素（Ｔｅｔｒｏｄｏｔｏｘｉｎ，ＴＴｘ）后对上述指标的影响。结果示，ＶＩＰ、ＰＧＥ２、ｄｂ－ｃＡＭＰ和ＥＦＳ均刺激ＨＣＯ３－分泌和Ｉｓｃ、ＰＤ的升高，而缺氧、缺钠和哇巴因呈抑制作用。ＤＩＤＳ和缺氯则完全抑制由ＰＧＥ２引起的刺激作用，部分抑制（５０％）由ＶＩＰ的刺激作用，而对ｄｂ－ｃＡＭＰ则无抑制作用。ＴＴＸ抑制由ＥＦＳ引起的作用。ＨＣＯ３－分泌与ＶＩＰ、ＰＧＥ２及ｄｂ－ｃＡＭＰ引起的细胞内ｃＡＭＰ水平不成正相关。
The purpose of this experiment was to investigate the regulation of HCO3-secretion and its ion channels for transport. The proximal duodenum of the white rabbits was taken and placed in the Ussing Chamber. The levels of VIP, PGE2, db-cAMP and electrical stimulation EFS) on the secretion of bicarbonate (HCO3-), the current (Isc) and the potential difference (PD), as well as hypoxia, lack of chlorine, sodium deficiency and DIDS (4,4-diisothiocyanostilbene- disulfonicacid, Ouabain and Tetrodotoxin (TTx) on these indexes. The results showed that VIP, PGE2, db-cAMP and EFS stimulated HCO3-secretion and Isc, PD increased, and hypoxia, sodium deficiency and ouabain was inhibited. DIDS and lack of chlorine completely inhibited the stimulatory effects caused by PGE2, partial inhibition (50%) stimulated by VIP, but no inhibition of db-cAMP. TTX suppresses the effects caused by EFS. HCO3-secretion and VIP, PGE2 and db-cAMP caused by intracellular cAMP levels are not positively correlated.