The relationship between hypoxic pulmonary vasoconstriction and arterial oxygen tension in the intact dog.

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Abstract
The relationship between the magnitude of hypoxic pulmonary vasoconstriction (hpv) and arterial O2 tension (PaO2) was studied in intact anesthetized dogs. Radioactive 133Xe was infused continuously into the inferior vena cava. A tracheal divider made it possible to vary the inspired gas composition to each lung independently. With constant ventilation the 133Xe in the mixed expired gas from each lung was proportional to the blood flow to that lung. Unilateral ventilation of the left lung with 7% O2 produced a diversion of blood flow away from the lung and a reduction in PaO2. Repeated hypoxic stimuli produced a progressively greater reduction in the blood flow to the hypoxic lung and a progressive increase in PaO2. Administration of a .beta.-adrenergic agonist, dobutamine hydrochloride, during ventilation of the left lung with 7% O2, resulted in an increased blood flow to the left lung and a further decrease in PaO2. Addition of CO2 to the inspired gas resulted in an increased diversion of blood flow away from the hypoxic lung but a decrease in PaO2. Respiratory alkalosis induced by over-ventilation decreased the hypoxic vasoconstriction and increased PaO2 slightly. Acid-base changes induced by infusion of 1 N lactic acid or 8.4% NaHCO3 had no significant effects on the magnitude of the hypoxic vasoconstriction, or on PaO2, during hypoxic ventilation of the left lung. The magnitude of hypoxic vasoconstriction and PaO2 in the experiments described above were positively correlated (r = 0.885), showing that the vasoconstriction may help to maintain PaO2. Apparently, the effects of CO2 on hpv and PaO2 may be explained largely by the changes in alveolar O2 pressure (PAO2) which are secondary to changes in PACO2.