ACID-SECRETION IN ISOLATED GUINEA-PIG COLON
ACID-SECRETION IN ISOLATED GUINEA-PIG COLON
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DOI：
10.1152/ajpgi.1987.253.2.g155
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发表时间：
1987-08-01
影响因子：
--
通讯作者：
KANEKO, K
中科院分区：
文献类型：
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作者：
SUZUKI, Y;KANEKO, K
分离的豚鼠远端结肠以1.0-1.5 μ mol·cm·dot的速率将酸分泌到粘膜浴溶液中。cm-2.cntdot. h ~（-1）时，将制备物安装在Ussing室中，并用无HCO_3-CO_2溶液浸泡。通过pH stat系统测量溶液的酸化和碱化速率，或根据溶液pH的变化计算。酸分泌主要集中在结肠的中段和远端，而近端和盲肠无酸分泌。粘膜酸化伴随着血清碱化，后者的速率约为0.4%。前者的60%。碳酸酐酶抑制剂醋甲唑胺（10-4 M），降低粘膜酸化和血清碱化率的幅度相似。粘膜酸化完全取消粘膜K+-无条件，但不受粘膜Na+-无条件。将哇巴因加入到粘膜溶液中立即抑制酸分泌。抑制的剂量依赖性符合Michaelis-Menten方程，在4 × 10 - 6时具有半最大效应。10-6 M.当粘膜溶液的pH降低到4.3时，粘膜酸化的速率基本上保持与pH = 7.4时相同。向粘膜和血清溶液中加入钒酸盐（10-4）可显著降低粘膜酸化速率。这些结果表明，来自上皮代谢的CO2被细胞中的碳酸酐酶水合，释放的H+进入粘膜溶液，而HCO 3-进入血清溶液。对哇巴因敏感的H ~+-ATP酶可能介导H ~+穿过粘膜。
Isolated guinea pig distal colons secreted acid into the mucosal bathing solution at a rate of 1.0-1.5 .mu.mol .cntdot. cm-2 .cntdot. h-1 when the preparations were mounted in Ussing chambers and bathed with HCO3--CO2-free solutions. The rates of the acidification and alkalinization of the solutions were measured by a pH stat system or calculated from changes in the pH of the solution. The acid secretion was localized in the middle and distal parts of the colon but absent in the proximal part of the colon and the cecum. The mucosal acidification was accompanied by serosal alkalinization, the rate of the latter being .apprx. 60% of the former. A carbonic anhydrase inhibitor, methazolamide (10-4 M), reduced both the mucosal acidification and serosal alkalinization rates by a similar magnitude. The mucosal acidification was completely abolished by mucosal K+-free conditions but unaffected by mucosal Na+-free conditions. Ouabain added to the mucosal solution promptly inhibited the acid secretion. Dose dependency of the inhibition conformed to the Michaelis-Menten equation with a half-maximal effect at 4 .times. 10-6 M. When the pH of the mucosal solution was reduced to 4.3, the rate of the mucosal acidification remained essentially the same as that at pH = 7.4. Vanadate (10-4) added to both the mucosal and serosal solutions significantly reduced the mucosal acidification rate. These results suggest that CO2 derived from the epithelial metabolism is hydrated by carbonic anhydrase in the cell and released H+ enters the mucosal solution while HCO3- enters the serosal solution. H+ exit across the mucosal membrane may be mediated by H+-ATPase that is sensitive to ouabain.