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作者旨在探讨代谢性酸中毒时脑脊液（ＣＳＦ）［ＨＣＯ－３］与ＰＣＯ２的相互关系。两组代谢性酸中毒模型均由静脉内输入０．２ｍｏｌ／ＬＨＣＩ产生，［ＨＣＯ－３］ａ１ｈ内下降到（１２２）ｍｍｏｌ／Ｌ。实验６ｈ时ＣＳＦ［ＨＣＯ－３］：１组（正常碳酸血性代酸）下降了１．６ｍｍｏｌ／Ｌ；组（低碳酸血性代酸）下降了７．０ｍｍｏｌ／Ｌ．ＣＳＦ［ＨＣＯ－３］与ＣＳＦＰｃｏ２，显著正相关（ｒ＝０．８３４，Ｐ＜０．０ｌ）．结果说明代谢性酸中毒时ＣＳＦ［ＨＣＯ－３］并不受［ＨＣＯ－３］ａ的明显影响，主要取决于ＣＳＦＰｃｏ２的变化，其调节机制与脉络丛上皮细胞内ＣＯ２的水化作用和ＣＡ活性有关。
The aim of this study was to investigate the relationship between cerebrospinal fluid (CSF) [HCO-3] and PCO2 in metabolic acidosis. Metabolic acidosis in both groups was induced by intravenous infusion of 0.2 mol / LHCI and decreased to (122) mmol / L within [HCO-3] a1h. In the experiment 6h CSF (HCO-3): 1 group (normal carbonic acid) decreased 1.6mmol / L; group (hypocapnic acid) decreased 7.0mmol / L. There was a significant positive correlation between CSF [HCO-3] and CSFPco2 (r = 0.834, P <0.01). The results indicate that metabolic acidosis, CSF [HCO-3] is not significantly affected by [HCO-3] a, mainly depends on changes in CSFPco2, its regulation mechanism and choroid plexus CO2 hydration and CA activity related.