Javaheri S
J Appl Physiol (1985). 1987 Apr;62(4):1582-8. doi: 10.1152/jappl.1987.62.4.1582.
We hypothesized that inhibition of carbonic anhydrase in the central nervous system by acetazolamide should limit the rise in cisternal cerebrospinal fluid (CSF) [HCO3-] observed in metabolic alkalosis. To test this hypothesis, isosmotic isonatremic metabolic alkalosis was produced in two groups of anesthetized, paralyzed, and mechanically ventilated dogs (8 in each group). Group II animals received 50 mg/kg of acetazolamide intravenously 1 h before induction of metabolic alkalosis of 5-h duration. Renal effects of acetazolamide were eliminated by ligation of renal pedicles. In both groups cisternal CSF [Na+] remained relatively constant during metabolic alkalosis. In group I CSF [Cl-] decreased 3.6 and 8.2 meq/l, respectively, 2.5 and 5 h after induction of metabolic alkalosis. Respective increments in CSF [HCO3-] were 3.4 and 6.0 meq/l. In acetazolamide-treated dogs, during metabolic alkalosis, increments in CSF [HCO3-] (4.8 and 7.2 meq/l, respectively, at 2.5 and 5 h) and decrements in CSF [Cl-] (9.1 and 13.3 meq/l) were greater than those observed in group I. We conclude that, in dogs with metabolic alkalosis and bilateral ligation of renal pedicles, acetazolamide impairs CSF regulation of HCO3- and Cl- ions; acetazolamide not only failed to impede HCO3- rise but actually appeared to increase it. The mechanisms for these observations are discussed.
我们假设，乙酰唑胺对中枢神经系统碳酸酐酶的抑制作用应能限制在代谢性碱中毒时观察到的脑池脑脊液（CSF）[HCO₃⁻]升高。为验证这一假设，在两组麻醉、麻痹并机械通气的犬（每组8只）中诱发等渗等钠代谢性碱中毒。第二组动物在诱发持续5小时的代谢性碱中毒前1小时静脉注射50mg/kg乙酰唑胺。通过结扎肾蒂消除乙酰唑胺的肾脏效应。在两组中，代谢性碱中毒期间脑池CSF[Na⁺]保持相对恒定。在第一组中，代谢性碱中毒诱发后2.5小时和5小时，CSF[Cl⁻]分别下降3.6和8.2mEq/L。CSF[HCO₃⁻]相应升高3.4和6.0mEq/L。在接受乙酰唑胺治疗的犬中，代谢性碱中毒期间，CSF[HCO₃⁻]升高（2.5小时和5小时分别为4.8和7.2mEq/L）以及CSF[Cl⁻]下降（9.1和13.3mEq/L）均大于第一组观察到的变化。我们得出结论，在患有代谢性碱中毒且双侧结扎肾蒂的犬中，乙酰唑胺损害CSF对HCO₃⁻和Cl⁻离子的调节；乙酰唑胺不仅未能阻止HCO₃⁻升高，实际上似乎还使其增加。讨论了这些观察结果的机制。
