Pulmonary lymph drains into the thoracic duct and then into the systemic venous circulation. Since systemic venous pressure (SVP) must be overcome before pulmonary lymph can flow, variations in SVP may affect lymph flow rate and therefore the rate of fluid accumulation within the lung. The importance of this issue is evident when one considers the variety of clinical interventions that increase SVP and promote pulmonary edema formation, such as volume infusion, positive-pressure ventilation, and various vasoactive drug therapies. We recorded pulmonary arterial pressure (PAP), left atrial pressure (LAP), and SVP in chronic unanesthetized sheep. Occlusion balloons were placed in the left atrium and superior vena cava to control their respective pressures. The superior vena caval occluder was placed above the azygos vein so that bronchial venous pressure would not be elevated when the balloon was inflated. Three-hour experiments were carried out at various LAP levels with and without SVP being elevated to 20 mmHg. The amount of fluid present in the lung was determined by the wet-to-dry weight ratio method. At control LAP levels, no significant difference in lung fluid accumulation could be shown between animals with control and elevated SVP levels. When LAP was elevated above control a significantly greater amount of pulmonary fluid accumulated in animals with elevated SVP levels compared with those with control SVP levels. We conclude that significant excess pulmonary edema formation will occur when SVP is elevated at pulmonary microvascular pressures not normally associated with rapid fluid accumulation.

No abstract

Lymph vessels branch and interconnect in a manner similar to a complex electronic circuit. Accordingly, we have applied circuit analysis techniques to the analysis of lymphatic systems. A lymph vessel is cannulated and the "equivalent circuits" are determined for the parts of the vessel upstream and downstream of the site of cannulation. Each equivalent circuit consists of a single resistor in series with a single pressure source. A diode is included to represent the lymphatic valves. The lymph flow rate may be determined by calculating the flow in the circuits when they are connected to each other. This technique can be applied to larger lymph trunks that receive lymph from many tissues.

We used a gravimetric technique to test for increased pulmonary capillary permeability after Escherichia coli endotoxin infusion in unanesthetized sheep. The sheep were chronically prepared with cannulas placed into the left atrium and pulmonary artery 1-2 wk before the experiments. We estimated pulmonary capillary pressure (Pc) as the average of pulmonary arterial and left atrial pressures, and used the modified method of Pierce to estimate the ratio of extravascular fluid weight (EVF) to blood-free dry weight. In 15 sheep we inflated a left atrial balloon to raise Pc to -10.7, 5, 10, or 15 mmHg above plasma oncotic pressure (IIc) for 3 h, then measured EVF. EVF averaged 4.0 +/- 0.2 (base line), 4.3 +/- 0.1, 4.5 +/- 0.1, and 5.1 +/- 0.5 (SD), respectively, for the four levels of Pc - IIc. We gave seven additional sheep 1 microgram/kg of E. coli endotoxin (0127:B8) and measured EVF after 3 h of stable Pc. Endotoxin increased Pc in each sheep. EVF was higher than control for the endotoxin sheep with Pc - IIc greater than -1. This finding is consistent with an increase in pulmonary capillary permeability caused by endotoxin. However, EVF was not elevated in the endotoxin sheep with Pc - IIc less than 1 mmHg. This shows that the increased permeability was insufficient to cause edema unless Pc was elevated. Thus endotoxin may cause edema by two mechanisms, 1) an increase in capillary permeability, and 2) an increase in Pc.

Cardiogenic pulmonary edema is caused by the increase in left atrial pressure when the left heart fails. The increased pressure causes rapid fluid accumulation within the lung interstitial spaces. However, over the following days to weeks, additional fluid may accumulate due to the deposition of excess lung connective tissue.