Nattie E E, Tenney S M
Am J Physiol. 1976 Aug;231(2):579-87. doi: 10.1152/ajplegacy.1976.231.2.579.
We have examined the effect of K depletion on CSF [HCO3-] homeostasis in awake rats. The relationship of CSF [HCO3-] to arterial [HCO3-] in metabolic acid-base disturbances is displaced is an upward direction and has a significantly increased slope in K-depleted vs. control rats (0.51 +/- 0.02 vs. 0.42 +/- 0.02). Results of partial K-repletion experiments, with peripheral acid-base balance held constant, suggest that the effect is K specific. The K-depleted animals also exhibit a wider (CSF-arterial) PCO2 difference than controls (11.1 vs. 8.4 mmHg). When CSF [HCO3-] is shown as a function of CSF PCO2 the data of K-depleted rats are no longer displaced when compared to controls but still have a significantly greater slope (1.21 +/- 0.23 vs. 0.89 +/- 0.08). This increased slope is interpreted to reflect enhanced HCO3- movement from blood to CSF at high arterial [HCO3-]. Analysis of our data and observations from the literature in conditions of mixed acid-base disturbances suggest that CSF [HCO3-] is determined by a) CSF PCO2 and b) the level of arterial [HCO3-] when the latter is greater than the normal CSF [HCO3-].
我们研究了钾缺乏对清醒大鼠脑脊液[HCO₃⁻]稳态的影响。在代谢性酸碱紊乱中，脑脊液[HCO₃⁻]与动脉血[HCO₃⁻]的关系向上移位，且与对照大鼠相比，钾缺乏大鼠的斜率显著增加（分别为0.51±0.02和0.42±0.02）。在维持外周酸碱平衡恒定的部分补钾实验结果表明，该效应具有钾特异性。钾缺乏的动物与对照相比，还表现出更宽的（脑脊液 - 动脉血）PCO₂差值（分别为11.1和8.4 mmHg）。当将脑脊液[HCO₃⁻]表示为脑脊液PCO₂的函数时，与对照相比，钾缺乏大鼠的数据不再移位，但斜率仍显著更大（分别为1.21±0.23和0.89±0.08）。这种增加的斜率被解释为反映了在高动脉血[HCO₃⁻]时，HCO₃⁻从血液向脑脊液的转运增强。对我们的数据以及文献中关于混合性酸碱紊乱情况的观察结果进行分析表明，脑脊液[HCO₃⁻]由以下因素决定：a）脑脊液PCO₂，以及b）当动脉血[HCO₃⁻]水平高于正常脑脊液[HCO₃⁻]时的动脉血[HCO₃⁻]水平。
