Interaction of PVO2 with PAO2 on hypoxic pulmonary vasoconstriction.

We tested the hypothesis that decreases in alveolar O2 pressure (PAO2) of a large lung compartment would, through decreases in arterial O2 pressure (PaO2) and mixed venous O2 pressure (PVO2), result in decreases in PAO2 of the remaining small lung compartment; thus large-compartment hypoxic pulmonary vasoconstriction (HPV) would be accompanied by concomitant small-compartment HPV. In eight pentobarbital-anesthetized dogs, whose left lower lobe (LLL) inspired oxygen concentration (FIO2) was constantly 0.21, selective stepwise reductions in the rest of the lung (RL) FIO2 from 1.0 to 0.15 caused the electromagnetically measured LLL blood flow (QLLL/Qt), pulmonary vascular resistance of RL (PVRRL), and PVRLLL to increase while RL PAO2, PaO2, PVO2, and LLL PAO2 progressively decreased. Stepwise reductions in RL FIO2 from 0.15 to 0.06 caused QLLL/Qt and PVRRL to decrease, PVRLLL To further increase, while RL PAO2, PaO2, PVO2, and LLL PAO2 progressively decreased further. Based on previously established PAO2 levels of maximum HPV gain and LLL dose-response curves, the RL FIO2-induced changes in QLLL/QT can be explained by different rates of change in RL and LLL PAO2 and PVR. Thus, our findings indicate that if decreases in RL FIO2 cause, in turn, large decreases in PaO2, PVO2 and "normoxic" lung PAO2, then PVO2 is an important determinant of the magnitude of the HPV response.

Potentiation of lobar hypoxic pulmonary vasoconstriction by intermittent hypoxia in dogs.

Based on previous whole lung findings, the authors tested the hypothesis that lobar hypoxic pulmonary vasoconstriction (HPV) would be potentiated by repeated intermittent lobar hypoxic challenges. In sixteen open-chested pentobarbital-anesthetized dogs they found that repetitive hypoxia of the left lower lobe (LLL) (Group I = LLL nitrogen ventilation, n = 8; Group II = LLL absorption atelectasis, n = 8) caused the percentage decrease in the electromagnetically measured fraction of the cardiac output perfusing the LLL (QLLL/Qt) to become progressively greater (increased LLL HPV) through the first three hypoxic challenges in Group I and through the first four hypoxic challenges in Group II. In four dogs in each group, after eight sequential hypoxic challenges with the initial standard method had been performed, the alternative method was performed three times. There was no significant difference between the eighth LLL HPV response and the subsequent three. These findings indicate that 1) the mechanism of blood flow decrease to atelectatic lung is probably the same as for nitrogen-ventilated lung, namely, by HPV, and 2) in order to maximize HPV in the nonventilated lung during one lung ventilation, several repeated intermittent cycles of deflation-inflation to the lung should be performed during the initiation of one lung ventilation.

Atelectatic lobe blood flow: open vs. closed chest, positive pressure vs. spontaneous ventilation.

We measured lobar hypoxic pulmonary vasoconstriction (HPV) caused by both absorption atelectasis (AA) and nitrogen ventilation (N2) during conditions of a) open chest and positive-pressure ventilation (PPV), b) closed chest ad PPV, and c) closed chest and spontaneous ventilation (SV) and compared conditions a with b and b with c. In eight pentobarbital-anesthetized dogs we found that selective hypoxia of the left lower loe (LLL) caused by either AA or N2 resulted in the same percent decrease in the electromagnetically measured LLL blood flow whether the ches was open or closed to whether ventilation was by PPV or SV (range 58.3-65.0%). Whether the chest was open or closed and whether ventilation was by PPV or SV, reexpansion and ventilation of LLL AA with LLL N2 did not change LLL blood flow and indicated that there were no mechanical forces responsible for the decreased LLL AA blood flow. Differences in the degree of hypoxia, magnitude of transpulmonary pressure, and absolute pulmonary vascular pressure between LLL AA and N2 were considered to be minor. We conclude that the mechanism of decreased blood flow to an atelectatic lobe, whether the chest is open or closed and whether ventilation is by PPV or SV, is entirely due to HPV.