Vogh B P, Maren T H
Am J Physiol. 1975 Mar;228(3):673-83. doi: 10.1152/ajplegacy.1975.228.3.673.
Rate constants have been determined for the entry of 22Na+, 36Cl minus, and H14CO3- into CSF from plasma in cats during changes in Pco2 with and without inhibition of carbonic anhydrase. The application of these rate constants to movement of unlabeled electrolytes suggests that Na+ and Cl minus enter CSF by a one-way flux into newly formed fluid, but that entering HCO3-is involved both in net accumulation in new fluid and in rapid exchange with existing HCO3-. The entering HCO3-ions are not transferred from plasma but are formed in secretory cells from dissolved CO2. The exchange component of HCO3-entry is Pco2-dependent; entry of Na+ and Cl minus is not; hence net rate of HCO3-formation estimated by difference between Na+ and Cl minus is not Pco2 dependent. The net rate of HCO3-formation lies within the availability of CO2 from blood flow to choroid plexus but is not necessarily limited to this tissue. When carbonic anhydrase is inhibited, the net rate of formation of HCO3-is close to the calculated uncatalyzed rate expected for choroid plexus. The entry of all three ions is reduced by carbonic anhydrase inhibition, but the enzyme does not seem to provide the primary signal for alteration of CSF acid-base status. Regulation of CSF pH appears to be achieved through changes in HCO3-concentration that occur subsequent to the secretion of HCO3--rich new fluid.
在有或没有碳酸酐酶抑制的情况下，当猫的二氧化碳分压（Pco2）发生变化时，已测定了22Na+、36Cl-和H14CO3-从血浆进入脑脊液（CSF）的速率常数。将这些速率常数应用于未标记电解质的移动表明，Na+和Cl-通过单向通量进入新形成的液体从而进入脑脊液，但进入的HCO3-既参与新液体中的净积累，也参与与现有HCO3-的快速交换。进入的HCO3-离子不是从血浆转移而来，而是在分泌细胞中由溶解的CO2形成。HCO3-进入的交换成分依赖于Pco2；Na+和Cl-的进入则不依赖；因此，通过Na+和Cl-之间的差异估计的HCO3-形成净速率不依赖于Pco2。HCO3-形成的净速率处于从血流到脉络丛的CO2可利用范围内，但不一定局限于该组织。当碳酸酐酶被抑制时，HCO3-的净形成速率接近脉络丛预期的计算出的无催化速率。碳酸酐酶抑制会降低所有三种离子的进入，但该酶似乎不是脑脊液酸碱状态改变的主要信号。脑脊液pH值的调节似乎是通过在富含HCO3-的新液体分泌后发生的HCO3-浓度变化来实现的。
