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本文旨在探讨急性代酸时ＣＳＦｐＣＯ＿２在ＣＳＦ酸碱调节中的作用及其机制。４组急性代酸犬模型均由静脉内输入０．２ＮＨＣｌ产生，血浆［ＨＣＯ＿３－］ｌｈ内下降到１２±２ｍｍｏｌ／Ｌ，实验持续６ｈ。Ⅰ组控制ＰａＣＯ＿２常，６ｈ时ＣＳＦ［ＨＣＯ＿３－］下降了１．１ｍｍｏｌ／Ｌ；Ⅱ组自然呼吸，ＣＳＦｐＣＯ＿２伴随ＰａＣＯ＿２下降，６ｈ时ＣＳＦ［ＨＣＯ＿３－］下降了６．５ｍｍｏｌ／Ｌ；Ⅲ组机械通气，ＰａＣＯ＿２和ＣＳＦｐＣＯ２均迅速下降，６ｈ时ＣＳＦ［ＨＣＯ＿３－］下降了８．２ｍｍｏｌ／Ｌ；Ⅳ组控制ＰａＣＯ＿２正常，脑室注入乙酰唑胺，６ｈ时ＣＳＦ［ＨＣＯ＿３－］下降了１１．４ｍｍｏｌ／Ｌ。结果说明急性代酸时．ＣＳＦ［ＨＣＯ＿３－］取决于ＣＳＦｐＣＯ＿２。ＣＳＦＨＣＯ＿３－主要来源于ＣＮＳＣＯ＿２的水化作用，与ＣＡ活性显著相关。
This article aims to investigate the role of CSFpCO_2 in the acid-base regulation of CSF during acute acidosis and its mechanism. 4 groups of acute acidosis model were produced by intravenous infusion of 0.2NHCl, plasma [HCO 3] lh decreased to 12 ± 2mmol / L, the experiment lasted 6h. Group Ⅰ was controlled by PaCO 2, and CSF [HCO 3] decreased by 1.1 mmol / L at 6 h; Group Ⅱ spontaneously resuscitated; CSF pCO 2 decreased with PaCO 2 decrease; CSF [HCO 3 3-] decreased by 6 mmol / , PaCO_2 and CSFpCO2 decreased rapidly, and CSF [HCO_3-] decreased 8.2mmol / L at 6h. PaCO_2 was normal in group Ⅳ, acetazolamide was injected into ventricles and decreased 11.4mmol / L at 6h. The results show that when acute acidification. CSF [HCO_3-] depends on CSFpCO_2. CSFHCO 3 mainly comes from the hydration of CNSCO 2, which is significantly correlated with CA activity.