Mochizuki M, Niizeki K, Tamura M
Jpn J Physiol. 1981;31(3):331-44. doi: 10.2170/jjphysiol.31.331.
When blood in the pulmonary capillary is oxygenated in hypercapnic air, PCO2 in the red cell has been thought to exceed alveolar PCO2 due to the Haldane effect, inducing outward CO2 diffusion. As long as the inward CO2 diffusion and, consequently, HCO3- formation are prevented in the red cell, the CO2 gain in plasma is reduced down to the level predicted from a CO2 dissociation curve of separated plasma. Therefore, if the direction of the CO2 diffusion is not reversed during the contact time, the virtual venous PCO2 (PEq), where the CO2 loss due to the Haldane effect is balanced with the gain due to the venoalveolar PCO2 gradient, becomes higher than the oxygenated venous PCO2 in proportion to the CO2 difference between the true and separated plasma. In order to verify the validity of the above assumption, the PEq value was measured in normo- and hypercapnia by using the Defares' extrapolation method in six normal subjects. The results obtained revealed that the PEq estimated in hypercapnia was obviously higher than that in normocapnia. The above difference was significantly greater in normoxia than in hypoxia. Furthermore, it agreed fairly well with the theoretical difference presumed by taking the difference in CO2 content between separated and true plasma and the R. Q. effect on the alveolar gas volume into account, suggesting that the inward CO2 diffusion following the oxygenation reaction could be disregarded in normoxic hypercapnia.
当肺毛细血管中的血液在高碳酸血症的空气中进行氧合时,由于哈代效应,红细胞内的PCO2被认为超过肺泡PCO2,从而导致CO2向外扩散。只要阻止红细胞内的CO2向内扩散以及由此产生的HCO3-形成,血浆中CO2的增加量就会降低到根据分离血浆的CO2解离曲线预测的水平。因此,如果在接触时间内CO2扩散方向没有逆转,由于哈代效应导致的CO2损失与静脉-肺泡PCO2梯度导致的CO2增加达到平衡时的虚拟静脉PCO2(PEq),将比氧合静脉PCO2高出与真实血浆和分离血浆之间的CO2差异成比例的值。为了验证上述假设的有效性,采用德法雷斯外推法在6名正常受试者的正常和高碳酸血症状态下测量了PEq值。所得结果显示,高碳酸血症时估计的PEq明显高于正常碳酸血症时。上述差异在常氧状态下比低氧状态下显著更大。此外,考虑到分离血浆和真实血浆之间的CO2含量差异以及R.Q.对肺泡气体量的影响,该结果与推测的理论差异相当吻合,这表明在常氧高碳酸血症状态下,氧合反应后向内的CO2扩散可以忽略不计。