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牛蛙胃底黏膜使管腔碱化的机制。

Mechanism of luminal alkalinization by bullfrog fundic mucosa.

作者信息

Takeuchi K, Merhav A, Silen W

出版信息

Am J Physiol. 1982 Nov;243(5):G377-88. doi: 10.1152/ajpgi.1982.243.5.G377.

DOI:10.1152/ajpgi.1982.243.5.G377
PMID:6982623
Abstract

Metiamide-inhibited fundic mucosa of bullfrog secreted alkali (OH-) at 0.1-0.2 mueq.cm-2.h-1.OH- was abolished by dinitrophenol (DNP) and was decreased significantly by 4,4-didsothiocyano-2,2-disulfonate stilbene (DIDS), anoxia, or HCO3(-)-free nutrient solution. In Na+ solutions, increasing nutrient, [HCO3(-)] augmented OH- and Isc linearly while resistance (R) decreased. No such changes occurred in Na+-free nutrient solution. In all experiments, delta Isc was approximately 12 X delta OH. Replacement of Cl- in the secretory solutions or in the nutrient solutions had no significant influence on OH-. When Na+-free nutrient solutions and Cl--free secretory solutions were present, OH- decreased significantly (P less than 0.01). Increasing nutrient [Cl-] in the absence of secretory Cl- significantly (P less than 0.01) augmented OH- and Isc. In the absence of secretory Cl-, OH- and Isc were linearly related to varying nutrient [Cl-]. In tissues with nutrient solutions on the secretory side and vice versa, apparent OH- was 0.4-0.5 mueq.cm-1.h-1 and was dependent on secretory [HCO3(-)] but was not affected by DNP, DIDS, or replacement of Cl- on secretory or nutrient solutions. We conclude that 1) OH- secretion is dependent on nutrient HCO3(-) and Na+ and oxidative metabolism, 2) endogenous HCO3(-) does not contribute significantly, and 3) adequate tissue Cl- must be present for normal OH-.

摘要

甲硫米特抑制的牛蛙胃底黏膜以0.1 - 0.2微当量·厘米⁻²·小时⁻¹的速率分泌碱(OH⁻)。OH⁻分泌被二硝基酚(DNP)消除,并被4,4 - 二异硫氰酸 - 2,2 - 二磺酸芪(DIDS)、缺氧或无HCO₃⁻的营养液显著降低。在含Na⁺的溶液中,增加营养液中的[HCO₃⁻]会使OH⁻和短路电流(Isc)呈线性增加,而电阻(R)降低。在无Na⁺的营养液中未发生此类变化。在所有实验中,ΔIsc约为12×ΔOH。在分泌液或营养液中替换Cl⁻对OH⁻没有显著影响。当存在无Na⁺的营养液和无Cl⁻的分泌液时,OH⁻显著降低(P < 0.01)。在无分泌性Cl⁻的情况下增加营养液中的[Cl⁻]会显著(P < 0.01)增加OH⁻和Isc。在无分泌性Cl⁻时,OH⁻和Isc与不同的营养液[Cl⁻]呈线性相关。在分泌侧使用营养液而另一侧反之的组织中,表观OH⁻为0.4 - 0.5微当量·厘米⁻¹·小时⁻¹,且依赖于分泌性[HCO₃⁻],但不受DNP、DIDS影响,也不受分泌液或营养液中Cl⁻替换的影响。我们得出结论:1)OH⁻分泌依赖于营养液中的HCO₃⁻、Na⁺和氧化代谢;2)内源性HCO₃⁻贡献不大;3)正常的OH⁻分泌必须有足够的组织Cl⁻存在。

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