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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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