Effects of hypoxia, blood PCO2 and flow on O2 transport in excised rabbit lungs

In previous studies using isolated perfused rabbit lungs, an O-2 deficit measured by an alveolar gas-to-end capillary blood P-O2 difference (A-aD(O2)) was absent at blood flows ((Q)over dot) consistent with severe exercise. Thus factors such as (V)over dotA/(Q)over dot heterogeneity, shunt and diffusion limitation that contribute to an O-2 deficit in vivo were absent. Here we attempted to increase diffusion limitation to O-2 transport by reducing the equilibration coefficient D/(beta(Q)over dot), the ratio of the diffusing capacity (D) to the product of (Q)over dot and the capacitance coefficient (beta, the slope of the blood O-2 content-P-O2 curve). First, we used hypoxic (10% O-2) ventilation in conjunction with a low P (v) over bar(O2) (approximate to 25 mmHg) because beta is largest in this region of the O-2 dissociation curve. Second, we increased beta by decreasing blood P-CO2 which shifts the O-2 dissociation curve to the left (Bohr effect). Third, we increased (Q)over dot to three times control to reduce D/(Q)over dot. CO diffusing capacity was measured as a function of blood flow and blood P-O2. A deficit in O-2 transport as measured by a significant A-aD(O2) was measured only under conditions of hypoxia and high blood flow. The measured O-2 deficit matched the predictions from the equilibration coefficients D/(beta(Q)over dot) based on measurements of beta, D and (Q)over dot. (C) 1998 Elsevier Science B.V. All rights reserved.