Diffusion in avian lungs.

Abstract

Arterial PO2 in resting, normoxic avian lungs in not at the level of predicted for an ideal crosscurrent lung. In contrast to healthy alveolar lungs, such a reduction in efficiency of O2 exchange from optimal levels cannot be totally explained by ventilation/perfusion inequality, and the discrepancy is most likely related to diffusion resistances. The diffusing capacity of avian lungs (DLO2) will depend on: 1) stratification in the air capillaries, 2) blood-gas barrier morphology, 3) O2-Hb kinetics ( theta ), and 4) diffusive/perfusive conductance (D/ beta bQ) matching. Stratification in air capillaries, the membrane diffusing capacity, and time available in pulmonary capillaries for arterialization do not appear to be limiting at rest. D/ beta bQ inequality is expected in normoxic avian lungs but predictive models show that this should not limit O2 uptake. However, these resistances may interact in crosscurrent lungs or there may be other unknown diffusion limitations (e.g., theta ) to reduce PaO2 in birds. Recent morphologic evidence suggests DLO2 may increase in birds during exercise and V/Q and D/ beta bQ inequality would be expected to have less of an effect during hypoxia. Together, these factors may reconcile the relatively low PaO2 in resting birds at sea level and their ability to exercise at high altitudes.