Macherey H J, Petersen K U
Institut für Pharmakologie, Medizinischen Fakultät, Rheinisch-Westfälische Technische, Hochschule Aachen, Federal Republic of Germany.
Gastroenterology. 1989 Dec;97(6):1448-60. doi: 10.1016/0016-5085(89)90389-2.
The effects of HCO3- on transepithelial conductance of guinea pig (and, in some experiments, rabbit) duodenum have been investigated using stripped preparations in Ussing-type chambers. Initial conductance amounted to approximately 27 mS/cm2. In the presence of serosal or bilateral HCO3- (20 mM), it fell to approximately 15 mS/cm2 within 60 min. With mucosal HCO3- or HCO3- -free solutions, conductance decreased to only approximately 23 mS/cm2. In the absence of HCO3-, serosal but not mucosal addition of HCO3- prompted a steep conductance drop that was 50% complete within 6 min. These effects were the same in proximal and distal segments, whereas conductance levels in the latter were higher. The effects of HCO3- required serosal Na+; they were partly prevented or reversed by serosal ouabain (3 x 10(-5) M), furosemide (10(-3) M), and other loop diuretics, and indomethacin (10(-5) M). Serosal addition of prostaglandin E2 (10(-7) M, followed by 10(-6) M) reduced conductance from approximately 22 to approximately 17 mS/cm2. This effect required serosal HCO3- and the presence of indomethacin. 8-Br-cyclic adenosine monophosphate (10(-3)M, serosal side) mimicked the effects of prostaglandin E2. Indomethacin and prostaglandin E2 did not influence the secretory flux of HCO3- (approximately 0.5 mumol/cm2.h, pH-stat method). Our results assign a critical role to serosal HCO3- in the maintenance of a low tissue permeability, dependent on the availability of prostaglandins (cyclic adenosine monophosphate) and involving HCO3- access to the cell rather than secretion.
使用Ussing型小室中的剥离标本，研究了HCO₃⁻对豚鼠（在某些实验中还包括兔子）十二指肠跨上皮电导的影响。初始电导约为27 mS/cm²。在存在浆膜或双侧HCO₃⁻（20 mM）的情况下，60分钟内它降至约15 mS/cm²。使用黏膜HCO₃⁻或无HCO₃⁻的溶液时，电导仅降至约23 mS/cm²。在无HCO₃⁻的情况下，浆膜而非黏膜添加HCO₃⁻会促使电导急剧下降，6分钟内下降50%。近端和远端节段的这些效应相同，不过后者的电导水平更高。HCO₃⁻的效应需要浆膜Na⁺；浆膜哇巴因（3×10⁻⁵ M）、呋塞米（10⁻³ M）和其他袢利尿剂以及吲哚美辛（10⁻⁵ M）可部分阻止或逆转这些效应。浆膜添加前列腺素E₂（10⁻⁷ M，随后为10⁻⁶ M）可使电导从约22 mS/cm²降至约17 mS/cm²。此效应需要浆膜HCO₃⁻以及吲哚美辛的存在。8-溴环磷酸腺苷（10⁻³ M，浆膜侧）模拟了前列腺素E₂的效应。吲哚美辛和前列腺素E₂不影响HCO₃⁻的分泌通量（约0.5 μmol/cm²·h，pH计法）。我们的结果表明，浆膜HCO₃⁻在维持低组织通透性方面起关键作用，这取决于前列腺素（环磷酸腺苷）的可用性，且涉及HCO₃⁻进入细胞而非分泌。
