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Clinically, the development of pulmonary edema is frequently associated with an elevation of left atrial pressure. 1 However, overt pulmonary edema does not always occur with such pressure elevations, even when the plasma oncotic pressure is greatly exceeded. 2 It is conceivable that a dilatation of the pulmonary lymphatic system might remove fluid from the lung and prevent, or delay, the development of overt pulmonary edema. In experimental studies on the dog, it has been demonstrated that lymph flow from the lungs increased with an acute elevation of the pulmonary venous pressure 3 " 6 ; however, the quantity of lymph was small and apparently ineffective in preventing the development of pulmonary edema. The critical question, however, of the extent of the pulmonary lymph flow in chronic pulmonary edema remained unanswered. It was the purpose of the current study to determine what i*ole, if any, the lymphatics play in the prevention of chronic pulmonary edema. MethodsMongrel dogs were used in this study. The aninuils were anesthetized with intravenous sodium pentobnrbitnl (29 mg./Kg.), and a side-to-side 5 to 15-min. aorticocuvnl anastomosis was made immediately below the renal vessels by approximating and suturing the aorta and vena cava. Dogs not surviving moro than one month were excluded from the study. Thirty animals not included iu the experimental group were used for preliminary

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Lymph was collected from the right duct and thoracic duct of 13 dogs in which acute pulmonary edema was produced by partial obstruction of the left atrium by means of a balloon. Elevation of left atrial pressure to 30 mm. Hg resulted in an increase in thoracic duct flow within 30 minutes, followed by an increase in right duct flow within the next 15 minutes. Critical pulmonary edema became manifest approximately 30 minutes after the onset of increased right duct flow, and the dogs died in pulmonary edema approximately 90 minutes after inflation of the left atrial balloon, unless the left atrial pressure was reduced. The per cent of fluid in serial lung biopsies increased in the first biopsy taken 15 minutes after the elevation of left atrial pressure to 30 mm. Hg, and the increase was sustained, resulting in engorgement of the lungs unless the left atrial pressure was decreased. The small absolute increase in lymph from the right duct suggests that the lymphatics are unable to function significantly to relieve the pulmonary edema produced in the.se acute experiments, resulting in an overflow of fluid into the tracheobronchial tree. C41utamic oxalacetic transaminase showed marked increases in the lymph from the right duct but only modest increases in the lymph from the thoracic duct throughout the experiments. Pyruvic transaminase in lymph from the right and thoracic ducts was relatively unchanged.

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