HYPOXIC VASOCONSTRICTION IN BUFFER-PERFUSED RABBIT LUNGS

Isolated rabbit lungs were buffer-perfused under constant flow-conditions with separate control of alveolar (PA(O2)) and mixed venous (P (v) over bar(O2)) O-2 tension. Alveolar hypoxia caused an increase in pulmonary artery pressure (PAP) with sigmoidal dose-dependency. Erythrocytes increased the strength of the hypoxic pulmonary vasoconstriction (HPV). The contractile and vasorelaxant responses to the onset and release of alveolar hypoxia, respectively, occurred within seconds. Kinetics of the PAP increase, but not the magnitude of response, were related to the velocity of PA(O2) decline. In contrast, changes in P (v) over bar(O2) both in the absence and presence of erythrocytes, did neither provoke any presser response nor amplify the response to concomitant alveolar hypoxia. Repeatedly performed HPV manoeuvres revealed excellent reproducibility, and long-term alveolar hypoxia (90 min) provoked a biphasic presser response. We conclude that the isolated rabbit lung is a feasible model for the characterization of hypoxic vasoconstriction, with specific features hitherto not described for perfused lungs of other species.