Jankowska L, Grieb P
Am J Physiol. 1979 Mar;236(3):F220-5. doi: 10.1152/ajprenal.1979.236.3.F220.
Oxygen tension was measured in samples of blood and cisternal cerebrospinal fluid taken from anesthetized, paralyzed, and mechanically ventilated rabbits at various levels of arterial PO2. Cerebrospinal fluid oxygen tension (CSF PO2) was correlated with arterial PO2 (linear regression equation PCSFO2 = 0.2472 Pao2 + 42.34). During hypoxia CSF PO2 was higher than arterial PO2 in most experiments. These data can be attributed to the Bohr effect, which would increase the PO2 of the blood in choroid plexus capillaries as a result of its acidification. The acidification was suggested by Maren (Am. J. Physiol. 222: 885-889, 1972) to be a part of the ionic exchanges involved in cerebrospinal fluid formation. Such a mechanism may be of importance for supporting choroid plexus metabolism and function during hypoxia. This mechanism is most clearly seen in the rabbit.
在不同动脉血氧分压水平下，对麻醉、麻痹并机械通气的家兔采集血液样本和脑池脑脊液样本，测量其中的氧分压。脑脊液氧分压（CSF PO2）与动脉血氧分压相关（线性回归方程为PCSFO2 = 0.2472 Pao2 + 42.34）。在大多数实验中，缺氧期间脑脊液氧分压高于动脉血氧分压。这些数据可归因于波尔效应，由于脉络丛毛细血管血液酸化，该效应会使其中血液的氧分压升高。Maren（《美国生理学杂志》222: 885 - 889, 1972）认为这种酸化是脑脊液形成过程中离子交换的一部分。这种机制可能对缺氧期间支持脉络丛的代谢和功能具有重要意义。这种机制在兔子身上最为明显。
