Jennings D B, Chen C C
J Appl Physiol. 1975 Mar;38(3):382-8. doi: 10.1152/jappl.1975.38.3.382.
In resting conscious dogs physiological dead space was calculated using the Bohr equation and measurements of arterial and mixed expired carbon dioxide tension. Whenever dogs inhaled carbon dioxide mixtures (5-10%) that had normal or low oxygen concentrations, the calculated dead space became negative. This paradox was based on the fact that the mixed expired carbon dioxide tension in resting hypercapnic dogs. Under these circumstances carbon dioxide was produced from the lung as measured by gas analyses and blood analyses. By the lung as measured by gas analyses and blood analyses. By reasoning this implies that "alveolar" carbon dioxide tension was higher than pulmonary venous carbon dioxide tension. The negative carbon dioxide gradient persisted at 14 days of chronic hypercapnia and reverted to normal within 10 min of breathing air after chronic hypercapnia. These findings suggest that the exchange of carbon dioxide in the lung cannot be explained solely on the basis of passive diffusion.
在清醒的静息犬中，使用玻尔方程以及动脉血和混合呼出二氧化碳分压的测量值来计算生理死腔。每当犬吸入氧气浓度正常或较低的二氧化碳混合物（5%-10%）时，计算出的死腔就会变为负值。这种矛盾基于静息高碳酸血症犬混合呼出二氧化碳分压这一事实。在这些情况下，通过气体分析和血液分析测量发现，肺会产生二氧化碳。通过推理这意味着“肺泡”二氧化碳分压高于肺静脉二氧化碳分压。慢性高碳酸血症14天时，负二氧化碳梯度持续存在，慢性高碳酸血症后呼吸空气10分钟内恢复正常。这些发现表明，肺内二氧化碳的交换不能仅基于被动扩散来解释。
