EFFECTS OF HYPOXIA, BLOOD P-CO2 AND FLOW ON O-2 TRANSPORT IN EXCISED RABBIT LUNGS

In previous studies using isolated perfused rabbit lungs, an O-2 defic it 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 sev ere exercise. Thus factors such as (V)over dotA/(Q)over dot heterogene ity, shunt and diffusion limitation that contribute to an O-2 deficit in vivo were absent. Here we attempted to increase diffusion limitatio n 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 bl ood O-2 content-P-O2 curve). First, we used hypoxic (10% O-2) ventilat ion in conjunction with a low P (v) over bar(O2) (approximate to 25 mm Hg) because beta is largest in this region of the O-2 dissociation cur ve. Second, we increased beta by decreasing blood P-CO2 which shifts t he O-2 dissociation curve to the left (Bohr effect). Third, we increas ed (Q)over dot to three times control to reduce D/(Q)over dot. CO diff using 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 me asured O-2 deficit matched the predictions from the equilibration coef ficients D/(beta(Q)over dot) based on measurements of beta, D and (Q)o ver dot. (C) 1998 Elsevier Science B.V. All rights reserved.