Abstract
Unilateral pulmonary artery ligation in dogs causes focal hemorrhagic atelectasis, an increase in lung weight, and a decrease in ventilation volume within 3-7 days. Gas and saline quasi-static volume-pressure studies show that these areas cannot be inflated and that the pulmonary static recoil of the inflatable portions of the ligated lung is unchanged. Alveolar bubbles expressed from areas of grossly and microscopically normal lung are stable. Areas of normal lung remain after pulmonary artery ligation and a generalized change in alveolar surface forces was not observed. The data emphasize the focal nature of the hemorrhagic atelectasis following pulmonary artery occlusion.

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