Evidence for H+ secretion by the in vivo canine gallbladder.
Evidence for H+ secretion by the in vivo canine gallbladder.
复制标题
体内犬胆囊分泌 H 的证据。
DOI：
10.1016/0016-5085(87)90118-1
复制
发表时间：
1987
期刊：
影响因子：
29.4
通讯作者：
Moore,EW
中科院分区：
文献类型：
--
作者：
Rege,RV;Moore,EW
在人类和大多数其他物种中，胆囊内容物的pH值下降发生在胆汁浓缩期间。最近对兔子、豚鼠和Necturus胆囊的体外研究强烈表明，钠重吸收期间粘膜H+分泌，可能代表Na+/H+交换。目前在体内的研究是第一次尝试，以确定是否H+分泌胆囊可以证明在活体动物。禁食12-24小时后，从27只麻醉犬中获得胆囊胆汁;在可变牛磺胆酸盐输注期间，还从3只犬中获得12份胆总管胆汁样品。在胆总管胆汁中，观察到的范围如下：pH，7.3-7.85; CO2分压（Pco 2），21-32 mmHg;总CO2浓度（[TCO 2]），16.4-41.4 mM;总胆盐浓度（[TBS]），16-93 mM;和[Na]，153-192 mM。在胆囊胆汁中，相应的范围如下：pH，5.72-7.29; Pco 2，36-101 mmHg; [TCO 2]，1.21-15.5 mM; [TBS]，150-305 mM;和[Na]，199-266 mM。在所有样品中，[Na]与[TBS]线性相关。[TBS] = 180 mM时，二氧化碳分压从胆总管胆汁中的平均27.3 mmHg升高至胆囊胆汁中的>100 mmHg，然后随着[TBS]升高至>300 mM而下降至约36 mmHg。Pco 2峰值出现在pH约6.4-6.6时，然后随着pH降至约5.7而下降。胆汁与血浆Pco 2的比值从胆总管样本的平均1.08增加到胆囊样本的>2.0（pH值约为6.3），然后在完全浓缩的胆汁中下降到约1.0。如果胆汁中的高Pco 2值仅仅是由于组织CO2的产生，则可以预期整个Na+重吸收过程中Pco 2的持续增加。结果强烈表明H+分泌（HCO 3 −中和），因为峰值Pco 2发生在[TBS]仅约180 mM时，远在钠吸收完成之前。据推测，H+分泌可能对钙致石性有重要的有利影响，降低了含CaCO 3 −胆结石形成的可能性。
In humans and most other species, a decline in pH of gallbladder contents occurs during the concentration of bile. Recent in vitro studies in rabbit, guinea pig, andNecturusgallbladders have strongly suggested mucosal H+secretion during sodium reabsorption, presumably representing a Na+/H+exchange. The present in vivo studies are the first attempt to determine whether H+secretion by the gallbladder can be demonstrated in the living animal. Gallbladder bile was obtained from 27 anesthetized dogs after 12–24-h fasts; 12 samples of common duct bile were also obtained in 3 dogs during variable taurocholate infusion. In common duct bile, observed ranges were as follows: pH, 7.3–7.85; CO2partial pressure (Pco2), 21–32 mmHg; total CO2concentration ([TCO2]), 16.4–41.4 mM; total bile salt concentration ([TBS]), 16–93 mM; and [Na], 153–192 mM. In gallbladder bile, respective ranges were as follows: pH, 5.72–7.29; Pco2, 36–101 mmHg; [TCO2], 1.21–15.5 mM; [TBS], 150–305 mM; and [Na], 199–266 mM. In all samples [Na] was linearly related to [TBS]. Carbon dioxide partial pressure increased from a mean of 27.3 mmHg in common duct bile to >100 mmHg in gallbladder bile at [TBS] = 180 mM, then declined to ~36 mmHg as [TBS] increased to >300 mM. Peak Pco2occurred at pH ~6.4–6.6, then declined as pH decreased to ~5.7. Bile to plasma Pco2ratios increased from a mean of 1.08 in common duct samples to >2.0 in gallbladder samples at pH ~6.3, then declined to ~1.0 in fully concentrated bile. If the high Pco2values in bile were solely due to tissue CO2production, a sustained increase in Pco2throughout Na+reabsorption might be expected. The results strongly suggest H+secretion (HCO3−neutralization), as peak Pco2occurred when [TBS] was only about 180 mM, long before sodium absorption was complete. It is hypothesized that H+secretion may have important favorable effects on calcium lithogenicity, reducing the likelihood of the formation of CaCO3−containing gallstones.