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Temporary unilateral pulmonary artery occlusion resulted within 1 minute in a shift of tidal volume away from unperfused lungs in 14 anesthetized closed-chest dogs. The shift of ventilation was caused by bronchoconstriction following the decrease of CO2 on the occluded side. It was prevented by inhalation into that side of 6% CO2 in air, isoproterenol aerosol or 100% N2, but not by atropine or vagotomy. Airway resistance on the occluded side was doubled, and compliance fell 25%. Functional residual capacity fell variably (0–25%), and anatomic dead space decreased. When blood flow was restored, shunting was detected and ventilation returned slowly with normal inflation or immediately after hyperinflation of that lung. This suggests that terminal and respiratory bronchiolar smooth muscle constriction may lead to airway closure and atelectasis and that the gas exchange of the smooth muscle in smaller airways is carried out by direct diffusion to and from the airway rather than with blood. Submitted on June 9, 1960

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Hypoxemia in patients with "alveolar-capillary block syndrome" is believed to be due to a barrier to the diffusion of oxygen caused by thickened alveolar and capillary membranes (1, 2). Theoretical considerations indicate that thickened membranes should not result in a Po2 difference between alveolar gas and pulmonary capillary blood when patients with impaired diffusion breathe 100 per cent 02. Inhalation of 02, therefore, should always correct hypoxemia in patients in whom a barrier to diffusion is the only defect. The reasoning is as follows: inhalation of 02 at sea level raises alveolar Po2 to about 670 mm Hg, and the large initial Po2 difference between alveolar gas and blood entering the pulmonary capillaries (600 to 630 mm Hg) causes a rapid diffusion of 02 across even thickened alveolarcapillary membranes and prompt saturation of the hemoglobin (3, 4). After hemoglobin is saturated with 02, the 02 behaves like an inert gas and enters the blood only in physical solution and almost instantaneously, so that blood leaving the pulmonary capillaries is in equilibrium with the Po2 in the alveolar gas.Our original plan was to test this theory by measuring directly the arterial Po2 of patients with "pure" alveolar-capillary block syndrome while they were breathing pure 02. If the theory is correct (and if pulmonary artery-to-vein shunts are not increased in these patients) the arterial Po2 should equal that of healthy subjects breathing pure 02 (620 to 650 mm Hg). On analysis of our data we realized that the arterial hypoxemia in patients with alveolar-capillary block syndrome