Shibata H, Saitoh Y, Takahashi H, Okubo T
Bull Eur Physiopathol Respir. 1976 Mar-Apr;12(2):297-315.
Buffer mechanism of cerebrospinal fluid (CSF) against acute hypercapnia was studied in eighteen dogs. The dynamic response of CSF to a stepwise change of CO2 concentration in inspired gas (room air -- 6% CO2 -- 12% CO2) was observed in eleven dogs, maintaining each condition for two hours. The changes in CSF acidity were less than that in arterial blood, while increases of bicarbonate ion concentration [HCO3-] in CSF were more prominent. Apparent buffer values, delta[HCO3-]/deltapH, were calculated from the results in different levels of CO2 breathing : they were 22.7 slykes from room air to 6% CO2 (step 1), and 39.7 slykes from 6% to 12% CO2 (step 2). Similar experiments were performed in seven dogs, suppressing carbonic anhydrase activity by systemic administration of acetazolamide. Apparent buffer values of CSF were 14.4 slykes in step 1 and 16.0 slykes in step 2. From the result we conclude : 1) that the activity of buffer mechanism of CSF in respiratory acidosis is PCO2 dependent and becomes stronger when PCO2 of CSF increases ; 2) for the explanation of this characteristic buffer mechanism of CSF, participation of carbonic anhydrase is suggested for transport mechanism of bicarbonate ion into CSF.
在18只狗身上研究了脑脊液(CSF)对急性高碳酸血症的缓冲机制。在11只狗身上观察了脑脊液对吸入气体中二氧化碳浓度逐步变化(室内空气 - 6%二氧化碳 - 12%二氧化碳)的动态反应,每种情况维持两小时。脑脊液酸度的变化小于动脉血,而脑脊液中碳酸氢根离子浓度[HCO3-]的增加更为显著。根据不同水平二氧化碳呼吸的结果计算出表观缓冲值,即δ[HCO3-]/δpH:从室内空气到6%二氧化碳(步骤1)为22.7斯拉克斯,从6%到12%二氧化碳(步骤2)为39.7斯拉克斯。在7只狗身上进行了类似实验,通过全身给予乙酰唑胺抑制碳酸酐酶活性。脑脊液的表观缓冲值在步骤1为14.4斯拉克斯,在步骤2为16.0斯拉克斯。根据结果我们得出结论:1)呼吸性酸中毒时脑脊液缓冲机制的活性依赖于脑脊液二氧化碳分压(PCO2),且当脑脊液PCO2升高时变得更强;2)为了解释脑脊液这种独特的缓冲机制,提示碳酸酐酶参与了碳酸氢根离子进入脑脊液的转运机制。