Abstract
The absence of demonstrable lymphatics beyond the alveolar ducts 1 suggests a factor in the rapid development frequently characterizing pulmonary edema. In the following experiments this anatomical fact was put to a functional test.
In 4 dogs under nembutal anesthesia the thoracic duct was can-nulated one centimeter from the point of its entrance into the left subclavian vein. Following this, a Starling-Knowleton heart-lung preparation was made, and the thoracic duct tied off above the diaphragm. The cannula in the duct was connected with a saline-filled rubber tube terminating in a glass dropper, the tip of which was adjusted to lie on a plane about 2 cm below the lowest level of the thoracic duct in the chest. The effluent was received into a graduated tube and its volume measured over 15-minute periods. Care was taken to keep the cannula free from clots. In 2 experiments chlorazol fast pink was administered (100 mg/kilo), rendering the lymph noncoagulable, and obviating the danger of intravascular clotting.
Flow measurements were made until the pulmonary edema that develops spontaneously in the heart-lung preparation had assumed massive proportions. No increase in flow was noted as the edema developed, but rather a tendency to decrease as fluid was lost from the blood stream into the lungs. Addition of saline or fresh blood to the reservoir restored the flow temporarily.
Any lymph collected from the thoracic duct in the preparation employed in these experiments can come only from the left side of the heart and the left lung. Moreover, since the bronchial vessels are not being perfused, any pulmonary contribution must be made by the respiratory areas of the lung. But in view of the fact that flow was not augmented in spite of the development of massive pulmonary edema, it seems unlikely that alveolar tissue is provided with a mechanism for lymph drainage capable of conducting an appreciable flow.
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