Gurtner G H, Traystman R J
J Appl Physiol Respir Environ Exerc Physiol. 1979 Jul;47(1):67-71. doi: 10.1152/jappl.1979.47.1.67.
Five anesthetized dogs were made severely hypercapnic by stepwise addition of CO2 to their inspired air. Blood PCO2 levels greater than 400 Torr were reached. During hypercapnia, the steady-state end-tidal PCO2 (PaCO2) was always higher than the simultaneous measured arterial PCO2 (PaCO2). The mean ratio PaCO2/PACO2 was 0.861 +/- 0.01. These results are consistent with the predictions of the Charged Membrane Hypothesis, that gas-to-blood PCO2 differences should be directly proportional to the blood H+ activity. The results cannot be explained by delayed equilibration of CO2 between plasma and red blood cells. The latter hypothesis predicts that, under the conditions of these experiments, the PCO2 of arterial blood should be higher than the PCO2 of end-tibal gas. The blood HCO3- during hypercapnia did not increase as much as would be predicted if the blood were exposed to CO2 in vitro. This may reflect movement of blood HCO3- generated by the buffering of carbonic acid into intracellular compartments during hypercapnia.
对五只麻醉犬通过向其吸入气体中逐步添加二氧化碳使其严重高碳酸血症。达到了血液PCO₂水平大于400托。在高碳酸血症期间，稳态呼气末PCO₂（PETCO₂）总是高于同时测量的动脉PCO₂（PaCO₂）。平均PaCO₂/PETCO₂比值为0.861±0.01。这些结果与带电膜假说的预测一致，即气体与血液之间的PCO₂差异应与血液H⁺活性成正比。这些结果不能用血浆和红细胞之间二氧化碳的延迟平衡来解释。后一种假说预测，在这些实验条件下，动脉血的PCO₂应高于呼气末气体的PCO₂。高碳酸血症期间血液HCO₃⁻的增加量不如血液在体外暴露于二氧化碳时预测的那么多。这可能反映了在高碳酸血症期间，由碳酸缓冲产生的血液HCO₃⁻向细胞内区室的移动。
