REGULATION OF REGIONAL PERFUSION DISTRIBUTION IN LUNGS EFFECT OF REGIONAL OXYGEN CONCENTRATION

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Abstract
To study the effect of regional O2 concentration on regional perfusion distribution in the lungs, the right upper lobe of a dog was isolated in vivo by a balloon catheter and was artificially ventilated with N2, 10% O2 in N2, air, 40% O2 in N2, 60% O2 in N2, 100% O2 and 10% CO2 in air while the rest of the right lung and the left lung maintained spontaneous breathing of ambient air. Patterns of change in regional perfusion distribution in the right upper lobe according to the difference in O2 concentration in the exchange gas mixtures were similar in the 3 different experimental models, i.e., in the normal and the reimplanted, denervated right upper lobe ventilated under the tidal alveolar pressure range, and in the normal right upper lobe ventilated under a hyperinflated state due to the increased alveolar pressure. Hypoxic gas mixtures such as N2 and 10% O2 in N2 administered to induce alveolar hypoxia induced decreased perfusion distribution in the right upper lobe compared with air. Hyperoxic gas mixtures such as 40% O2 in N2, 60% O2 in N2 and 100% O2 induced alveolar hyperoxia and increased regional perfusion distribution. Perfusion partition to the right lung as a whole showed few, if any, changes due to the difference in O2 concentration in the exchange gas mixtures for the right upper lobe, indicating shifting of perfusion from the right upper lobe to the remainder of the right lung, and vice versa. Regional hypoxia possibly induced regional vasoconstriction, regional hyperoxia, regional vasodilation and/or recruitment of the pulmonary vascular beds. The O2 sensitivity of the pulmonary vascular bed decreased as the O2 concentration in the exchange gas mixtures exceeded 60%, or the alveolar PO2 exceeded 250 mm Hg. Pulmonary vascular responses to alveolar hypoxia and hyperoxia seem to be purely local phenomena, and nervous integrity is not essential.