Scheid P, Piiper J
Respir Physiol. 1980 Jan;39(1):1-31. doi: 10.1016/0034-5687(80)90011-0.
(1) The scope of this review is to examine the experimental evidence for the existence of negative PCO2 differences between pulmonary capillary blood and lung gas, [delta PCO2(b-G)], which have been observed both during rebreathing, when CO2 was at equilibrium, and during steady state gas exchange, particularly in hypercapnia. (2) The mechanism that have been invoked to explain negative delta PCO2(b-G) include (i) slow equilibration of the system CO2/HCO3-/H+ in blood, and (ii) effects of a negatvely charged surface of the pulmonary capillary endothelium. While the first postulated mechanism appears to be quantitatively insufficient to explain the results, the second seems to lead to serious qualitative difficulties. (3) Existence of negative delta PCO2(b-G) in CO2 equilibrium would invalidate the basis of the conventional analysis of alveolar gas exchange. (4) A critical analysis of the experimental evidence for the existence of negative delta PCO2(b-G) is presented. It includes the identification of directional experimental errors leading to spurious negative delta PCO2(b-G), and a critical review of the literature data in this regard. (5) Results of own experiments, conducted in an attempt to consider all possible sources of error, are reported, revealing (i) perfect PCO2 equality between alveolar gas and blood in rebreathing equilibrium of CO2; (ii) absence of negative delta PCO2 (b-G) during steady state gas exchange in hypercapnia. (6)Both experiments and model calculations show that negative delta PCO2 between mixed venous blood and end-expired gas observed in birds at steady state of gas exchange are explained by a particular action of the Haldane effect in avian parabronchial lungs with cross-current arrangement of gas and blood flow. (7) It is concluded that the negative delta PCO2(b-G) reported in the literature are probably artifactual and that there is no adequate evidence to invalidate the traditional view according to which blood/gas CO2 equilibration in lungs leads to equal PCO2 in both media.
(1)本综述的范围是研究肺毛细血管血液与肺气体之间存在负二氧化碳分压差值[ΔPCO₂(b - G)]的实验证据,这种差值在重复呼吸期间(此时二氧化碳处于平衡状态)以及稳态气体交换期间(特别是在高碳酸血症时)均有观察到。(2)被用来解释负ΔPCO₂(b - G)的机制包括:(i)血液中CO₂/HCO₃⁻/H⁺系统的缓慢平衡;(ii)肺毛细血管内皮带负电荷表面的影响。虽然第一种假设机制在数量上似乎不足以解释结果,但第二种机制似乎导致了严重的定性困难。(3)在二氧化碳平衡状态下存在负ΔPCO₂(b - G)将使传统肺泡气体交换分析的基础无效。(4)对存在负ΔPCO₂(b - G)的实验证据进行了批判性分析。其中包括识别导致虚假负ΔPCO₂(b - G)的方向性实验误差,以及对这方面文献数据的批判性综述。(5)报告了为考虑所有可能的误差来源而进行的自身实验结果,结果显示:(i)在二氧化碳重复呼吸平衡时,肺泡气体与血液中的PCO₂完全相等;(ii)在高碳酸血症稳态气体交换期间不存在负ΔPCO₂(b - G)。(6)实验和模型计算均表明,在气体交换稳态下鸟类混合静脉血与终末呼出气体之间的负ΔPCO₂是由哈代效应在具有气体和血流交叉排列的鸟类副支气管肺中的特殊作用所解释的。(7)得出的结论是,文献中报道的负ΔPCO₂(b - G)可能是人为造成的,并且没有充分的证据使传统观点无效,即肺部血液/气体二氧化碳平衡导致两种介质中的PCO₂相等。