脑脊液中碳酸氢根在高碳酸血症时的增加与脑中碳酸氢根、谷氨酸、谷氨酰胺和氨的关系。

The CSF HCO3 increase in hypercapnia relationshp to HCO3, glutamate, glutamine and NH3 in brain.

作者信息

Kazemi H, Wyen J, van Leuven F, Leusen I

出版信息

Respir Physiol. 1976 Dec;28(3):387-401. doi: 10.1016/0034-5687(76)90032-3.

Abstract

To study the role of carbonic anhydrase in the CSF [HCO3] increase in respiratory acidosis and its effect on brain ammonia, anesthetized rats were subjected to hypercapnia (7% CO2) for 2 hours. The animals received periodic intraventricular injections of either 'mock' CSF or 'mock' CSF and acetazolamide for 45 minutes prior and during hypercapnia when: (a) plasma [HCO3-] was allowed to increase normally and (2) plasma [HCO3] increase was prevented by i.v. HC1 infusion, CSF [HCO3] increased 8.5 mM/L after 2 hours of hypercapnia (delta PCO2 40) in the rats with intraventricular 'mock' CSF injections, and only 6 mM/L in the animals with acetazolamide injections. CSF [HCO3-] increased 7 mM/L during hypercapnia and HCl infusion with intraventricular 'mock' CSF injections, but only 2 mM/L with acetazolamide injections. Changes in total brain CO2 (increase) and brain glutamic acid (decrease) in hypercapnia were not affected by intraventricular acetazolamide and i.v. HCl. The increase of brain NH4+ and glutamine in hypercapnia was reduced in these conditions. It is concluded that there are at least two sources for the CSF [HCO3-] increase in hypercapnia; one formed in the CNS and dependent on carbonic anhydrase, and the other derived from plasma [HCO3-] increase.

摘要

为研究碳酸酐酶在呼吸性酸中毒时脑脊液[HCO₃⁻]升高中的作用及其对脑氨的影响，对麻醉大鼠进行2小时的高碳酸血症（7% CO₂）处理。在高碳酸血症之前及期间的45分钟内，给动物定期脑室内注射“模拟”脑脊液或“模拟”脑脊液与乙酰唑胺，当：（a）血浆[HCO₃⁻]正常升高时，以及（b）通过静脉输注盐酸防止血浆[HCO₃⁻]升高时，脑室内注射“模拟”脑脊液的大鼠在高碳酸血症2小时后（ΔPCO₂ 40）脑脊液[HCO₃⁻]升高8.5 mM/L，而注射乙酰唑胺的动物仅升高6 mM/L。在高碳酸血症和盐酸输注期间，脑室内注射“模拟”脑脊液时脑脊液[HCO₃⁻]升高7 mM/L，但注射乙酰唑胺时仅升高2 mM/L。高碳酸血症时全脑二氧化碳的变化（升高）和脑谷氨酸的变化（降低）不受脑室内乙酰唑胺和静脉注射盐酸的影响。在这些情况下，高碳酸血症时脑NH₄⁺和谷氨酰胺的升高有所降低。结论是，高碳酸血症时脑脊液[HCO₃⁻]升高至少有两个来源；一个在中枢神经系统中形成且依赖碳酸酐酶，另一个源自血浆[HCO₃⁻]的升高。