Anatomical backgrounds on gas exchange parameters in the lung

Figure 14 Relative contribution of 1/D_M and 1/D_B to overall resistance of 1/D_L. Difference in membrane diffusing capacity for CO (D_MCO) and that for NO (D_MNO) is simply attributed to difference in their Krogh diffusion constants defined as (α∙d), where α is Bunsen solubility coefficient of the gas (mL/mL/atm) and d is gas diffusivity (cm²/s) in alveolocapillary membrane and plasma layer. D_MNO/D_MCO is assumed to be 1.97[65]. On the other hand, blood-diffusing capacity for CO (D_BCO) or NO (D_BNO) is defined as alveolar capillary blood volume (V_C) multiplied by specific gas conductance of each gas (θ_CO, θ_NO). θ_CO signifies the diffusive process across erythrocyte membrane and its interior incorporated with the competitive, replacement reaction of CO with hemoglobin O₂. Therefore, θ_CO changes significantly depending on surrounding P_O2. On the other hand, θ_NO is not influence by chemical reaction with hemoglobin and is predominant by diffusion across erythrocytes, thus resulting in constant θ_NO [4.5 mL/min/mmHg/(mL×blood)[65,93]]. The pulmonary diffusing capacity for CO is primarily governed by both diffusion through alveolocapillary membrane and erythrocytes as well as reaction in erythrocytes (limitation by both diffusion and reaction), whereas the pulmonary diffusing capacity for NO is almost evenly prescribed by diffusion through alveolocapillary membrane and that inside erythrocytes (diffusion limitation only). Important message drawn from this analysis is that the pulmonary diffusing capacity for NO is evenly sensitive to morphological abnormality in alveolocapillary membrane as well as that in pulmonary microcirculation. On the other hand, the pulmonary diffusing capacity for CO is more sensitive to microcirculatory abnormality. Adopted from ref[65].