抄録
To investigate the buffer mechanism of cerebrospinal fluid in acute hypercapnia in vivo, we have studied the acid-base status of CSF in 14 mongrel dogs, changing their inspiratory CO2 concentration, from room air to 6% and then to 12%. Each condition was maintained for two hours, and at the end of each CO2 loading, arterial and CSF samples were taken anaerobically for the determination of PO2, PCO2, pH and [HCO3-] by electrode and Van Slyke-gas chromatograph system. Buffer values, Δ[HCO3-]/ΔpH were calculated for blood and CSF between room air and 6% CO2 breathing and also between 6% and 12% CO2 breathing.
As results, followings were concluded:
1) The buffer values of CSF in vivo in acute hypercapnia were significantly higher than those of arterial blood.
2) The buffer values of CSF increased significantly with increases of CSF PCO2.
3) An active transport system is presumably necessary for the explanation of this PCO2 dependent buffer mechanism, in which the participation of carbonic anhydrase would be suggested.
