LOCAL PULMONARY BLOOD-FLOW - CONTROL AND GAS-EXCHANGE

We studied the local response of the pulmonary vasculature to combined changes in alveolar P(O2) and P(CO2) in the right apical lobe (RAL) of six conscious sheep. That lobe inspired an O2-CO2-N2 mixture adjusted to produce one of 12 alveolar gas compositions: end-tidal P(CO2) (PET(CO2)) of 40, 50, and 60 Torr, each coupled with end-tidal P(O2) (PET(O2)) of 100, 75, 50, and 25 Torr. In addition, at each of the four PET(O2), the inspired CO2 was set to 0 and PET(CO2) was allowed to vary as RAL perfusion changed. The remainder of the lung, which served as control (CL) inspired air. Fraction of the total pulmonary blood flow going to the RAL (%QRAL) was obtained by comparing the methane elimination from the RAL to that of the whole lung, and expressed as a percentage of that fraction at PET(CO2) = 40, PET(O2) = 100. Cardiac output, pulmonary vascular pressures, and CL gas tensions were unaffected or only minimally affected by changes in RAL gas composition. A drop in P(O2) from 100 to 50 Torr decreased local blood flow by 60% in normocapnia and by 66% at a P(CO2) of 60. At all levels of oxygenation, an increase in P(CO2) from 40 to 60 reduced QRAL by nearly 50%. With these stimulus-response data, we developed a model of gas exchange, which takes into account the effects of test segment size on blood flow diversion. This model predicts that: (1) when the ventilation to one compartment of a two compartment lung is progressively decreased, PA(O2) remains above 60 Torr for up to 60% reductions in alveolar ventilation, irrespective of compartment size; (2) the decrease in PA(O2) that occurs at altitude is accompanied by a drop in PA(CO2) that limits the decrease in conductance and minimizes the pulmonary hypertension; and (3) as we stand, local blood flow control by the alveolar gas tensions halves the alveolar-arterial P(O2) and P(CO2) differences imposed by gravity.