Nattie E E
Respir Physiol. 1980 Jun;40(3):309-22. doi: 10.1016/0034-5687(80)90031-6.
Rats were exposed to 11% CO2 in air for 15 min or 3 h and measurements made of ventilation, CSF acid-base values, and blood, CSF and brain electrolytes. Brain tissue HCO3- was studied by performing CO2 titration curves of tissue homogenates in vitro, the upward displacement of these curves reflecting the non-physico-chemical buffer mechanisms prominent in sustained hypercapnia. At 15 min, the CO2 induced increase in [HCO3-] was accompanied in CSF by an equimolar increase in [Na+] and in brain tissue by an increase in [K+]. At 3 h, the further increase in [HCO3-] was accompanied in CSF by a smaller increase in [Na+] and a decrease in [Cl-] and in brain tissue, there were no longer any significant changes in monovalent ions. In brain, the immediate pH regulatory response to hypercapnia appears to involve physico-chemical buffering and an ionic exchange with blood while by 3 h, the further increase in cell HCO3- must reflect altered cell metabolism. In CSF, the immediate increase in [Na+] and [HCO3-] is probably via choroid plexus while by 3 h, the CSF [HCO3-] increase could reflect exchange with blood at non-choroidal sites or to a less likely extent exchange with brain cells. CSF and brain cell pH regulation is reflected in ventilation which is lower at 3 h than at 15 min of CO2 exposure.
将大鼠置于含11%二氧化碳的空气中15分钟或3小时，然后测量其通气量、脑脊液酸碱值以及血液、脑脊液和脑组织中的电解质。通过对体外组织匀浆进行二氧化碳滴定曲线研究脑组织中的HCO₃⁻，这些曲线的上移反映了在持续性高碳酸血症中突出的非物理化学缓冲机制。在15分钟时，二氧化碳诱导的[HCO₃⁻]升高在脑脊液中伴随着[Na⁺]等摩尔升高，在脑组织中伴随着[K⁺]升高。在3小时时，[HCO₃⁻]的进一步升高在脑脊液中伴随着[Na⁺]较小幅度升高和[Cl⁻]降低，在脑组织中，单价离子不再有任何显著变化。在大脑中，对高碳酸血症的即时pH调节反应似乎涉及物理化学缓冲和与血液的离子交换，而到3小时时，细胞内HCO₃⁻的进一步升高必定反映了细胞代谢的改变。在脑脊液中，[Na⁺]和[HCO₃⁻]的即时升高可能是通过脉络丛，而到3小时时，脑脊液中[HCO₃⁻]的升高可能反映了在非脉络丛部位与血液的交换，或者在较小程度上反映了与脑细胞的交换。脑脊液和脑细胞的pH调节反映在通气上，在二氧化碳暴露3小时时的通气量低于15分钟时的通气量。
