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

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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We measured the pulmonary lymph flow in dogs with mild congestive failure before and after acute elevation of the left atrial pressure to 40 cm of water. The creation of an aorticocaval fistula and the administration of desoxycorticosterone trimethylacetate and a salt enriched diet in 6 dogs produced mild pulmonary edema and partial expansion of the pulmonary lymphatics 10 to 12 days postoperatively. Elevation of the left atrial pressure to 40 cm of water under pentobarbital anesthesia led to an immediate increase in right duct flow in the "mild failure" dogs, in contrast to a delayed flow in normal dogs. The average peak flows in the 10-to 12-day dogs after increasing the left atrial pressure were higher than the peak flows observed in normal dogs. In addition, the mild failure dogs survived twice as long as normal dogs after acute elevation of the left atrial pressure. These results suggest that an animal with an expanded pulmonary lymph system is better able to withstand the stress of acute elevation of left atrial pressure than a normal animal. The pulmonary lymph system may serve as an important compensatory mechanism in the prevention of fulminating pulmonary edema. ADDITIONAL KEY WORDS lymphatic system (pulmonary) arteriovenous anastomosisedema desoxycorticosterone arteriovenous fistula lymph (pulmonary) pulmonary circulation pulmonary edema anesthetized dogs• Following the production of chronic pulmonary edema in dogs by our technique (1), the right duct lymphatics that drain the lung became markedly enlarged and a very large increase in right duct lymph flow occurred.Since only a limited augmentation in lymph flow occurred in acute pulmonary edema produced by elevating left atrial pressure to 40 cm of water (2), we suspected that a gradually developing expansion of the lymph system may play a role as a compensatory mechanism in chronic pulmonary edema, by From the facilitating the removal of critical accumulations of fluid from the lungs. The present experiment was designed to study pulmonary lymph flow and the course of events subsequent to acute elevation of the left atrial pressure in dogs with mild chronic pulmonary edema, whose lymphatics, presumably, have had a chance to partially expand, and in normal dogs subjected to the same acute elevation of left atrial pressure. It has been demonstrated that 10 days after initiation of procedures inducing chronic heart failure in the dog (3), right duct lymph flow began to increase significantly and presumably lymphatic expansion was well underway. Accordingly, the right duct lymph flow was recorded (4) before and after elevation of left atrial pressure at 40 cm of water by inflating a balloon (2) in the left atrium of 306

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