Heylings J R, Feldman M
Department of Internal Medicine, Veterans Administration Medical Center, Dallas, Texas.
Am J Physiol. 1988 Oct;255(4 Pt 1):G470-5. doi: 10.1152/ajpgi.1988.255.4.G470.
We studied basal and prostaglandin E2 (PGE2)-stimulated duodenal HCO3- transport in the rat in vivo both in the presence and absence of a concentration gradient for HCO3- from blood to lumen. Basal HCO3- transport was not reduced when the luminal solution was changed from one containing 0 mM HCO3- to one containing 22 mM HCO3- either at pH 9.0 or 7.5. Thus basal duodenal HCO3- transport in rats is independent of a blood-to-lumen HCO3- concentration gradient, which indicates an energy-dependent process with little passive flux of HCO3-. Luminal or intravenous administration of PGE2 significantly (P less than 0.01) increased HCO3- secretion into a HCO3(-)-free luminal solution but had no effect on HCO3- secretion into luminal solutions containing 22 mM HCO3-, either at pH 9.0 or 7.5. Therefore prostaglandins may act by increasing passive flux of HCO3- rather than by stimulating energy-dependent duodenal HCO3- transport.
我们研究了在存在和不存在从血液到肠腔的HCO₃⁻浓度梯度的情况下，大鼠体内基础状态以及前列腺素E₂（PGE₂）刺激的十二指肠HCO₃⁻转运。当管腔溶液在pH 9.0或7.5时从含0 mM HCO₃⁻的溶液变为含22 mM HCO₃⁻的溶液时，基础HCO₃⁻转运并未降低。因此，大鼠十二指肠基础HCO₃⁻转运不依赖于血液到肠腔的HCO₃⁻浓度梯度，这表明这是一个能量依赖过程，HCO₃⁻的被动通量很少。管腔内或静脉内给予PGE₂显著（P＜0.01）增加了HCO₃⁻向不含HCO₃⁻的管腔溶液中的分泌，但对向含22 mM HCO₃⁻的管腔溶液（pH 9.0或7.5）中的HCO₃⁻分泌没有影响。因此，前列腺素可能通过增加HCO₃⁻的被动通量起作用，而不是通过刺激能量依赖的十二指肠HCO₃⁻转运。
