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Myocardial edema formation, which has been shown to compromise cardiac function, and increased epicardial transudation (pericardial effusion) have been shown to occur after elevation of myocardial venous and lymphatic outflow pressures. The purposes of this study were to estimate the hydraulic conductance and osmotic reflection coefficient for the epicardium and to determine the effect of coronary sinus hypertension and cardiac lymphatic obstruction on epicardial fluid flux (JV,e/Ae). A Plexiglas hemispheric capsule was attached to the left ventricular epicardial surface of anesthetized dogs. JV,e/Ae was determined over 30-min periods for three intracapsular pressures (-5, -15, and -25 mmHg) and two intracapsular solutions exerting colloid osmotic pressures of 7.0 and 2.0 mmHg. Hydraulic conductance was estimated to be 3.7 +/- 0.5 microliters.h-1.cm-2.mmHg-1. An osmotic reflection coefficient of 0.9 was calculated from the difference in JV,e/Ae of 16.5 +/- 8.4 microliters.h-1.cm-2 between the two solutions. Graded coronary sinus hypertension induced a linear increase in JV,e/Ae, which was significantly greater in dogs without cardiac lymphatic occlusion than in those with occlusion.

We hypothesized that myocardial microvascular filtration rate (Jv) could be manipulated by varying end-diastolic myocardial interstitial hydrostatic (P(int)) pressure. Dogs under general anesthesia were instrumented with intramyocardial capsules to measure P(int) and with prenodal myocardial lymphatic trunk cannulas and superior vena caval balloon-tipped catheters to manipulate myocardial lymph flow. Because, for a given surface area, the lymph-to-plasma protein concentration ration (CL/CP) varies inversely with JV, CL/CP was utilized as an index of changes in JV. When lymphatic outflow pressure (P0) was elevated to abolish lymph flow and force myocardial interstitial fluid volume to expand, P(int) rose significantly from 15.0 +/- 0.8 to 27.6 +/- 1.0 mmHg and CL/CP increased significantly from 0.75 +/- 0.04 to 0.85 +/- 0.04, indicating a decrease in JV. When P0 was lowered and lymph flow resumed, P(int) and CL/CP decreased significantly to 15.3 +/- 0.9 mmHg and 0.75 +/- 0.04, respectively, indicating an increase in JV. We conclude that myocardial microvascular filtration rate may be modulated by changes in P(int) resulting from alterations in myocardial interstitial fluid volume secondary to variations in lymph flow from the heart.

The effect of superior vena caval pressure (SVCP) elevation on the formation of pleural effusions (PE) was studied in sheep. Through a right thoracotomy, a Silastic cuff was placed around the superior vena cava. Catheters for monitoring SVCP and pulmonary artery pressure (PAP) were also placed. After a 1- to 3-wk recovery period, we measured the SVCP, PAP, cardiac output, and plasma protein concentration (Cp). We then elevated the SVCP to various levels from base line [5.3 +/- 2.6 (SD) mmHg] to 33 mmHg. The cardiac output, PAP, and Cp were remeasured 1–2 h and 24 h after SVCP elevation. At the end of the 24-h period, the animals were killed. The PE volume and pleural fluid protein concentration (Cpl) were measured, and the Cpl/Cp was calculated. PE generally did not occur until the SVCP was elevated above 15 mmHg. To study the effect of the thoracotomy on the subsequent pleural effusion, we studied six additional sheep in which we did not perform a thoracotomy. In these animals, the SVCP was elevated to between 5 and 28 mmHg for 24 h by use of a 16-Fr balloon catheter placed via a left external jugular vein and a right carotid-external jugular shunt. We found that the PE volume, for a given SVCP elevation, was similar to that present in sheep that received a thoracotomy. For all sheep the volume of PE was related to SVCP by the equation PE (ml) = 0.24e0.26SVCP, r = 0.85. In the sheep without a thoracotomy, Cpl/Cp rose with increasing volume of PE. Our data demonstrate that elevation of SVCP greater than 15 mmHg for 24 h results in the formation of PE. The rise in Cpl/Cp with PE volume suggests that filtration through the pleural vessels is not the major contributor to PE formation.

We used a circuit-model technique to analyze the flow from intestinal lymphatics. Postnodal lymph vessels from the small intestine were cannulated in five halothane-anesthetized dogs. We measured the flow rate from the cannula (QL) as we held the outflow end of the cannula at several heights above the site of cannulation. At each cannula height we calculated the pressure at the outflow end of the lymphatic (Po) as Po = QL X cannula resistance + height of the outflow end of the cannula above the cannulation site. Then we determined a best-fit regression line for QL vs. Po. The effective lymphatic resistance (RL) was estimated from the regression line as -delta Po/delta RL and the effective pressure driving lymph flow (PL) was taken as the Po at which QL = 0. At base line, RL = 0.039 +/- 0.018 (SD) cmH2O.min.microliters-1 and PL = 5.2 +/- 2.4 cmH2O. When we raised the portal venous pressure from 11.4 +/- 4.0 cmH2O (base line) to 34.4 +/- 9.0 cmH2O, RL decreased by only 26 +/- 11%, but PL rose by 160% to 13.6 +/- 8.7 cmH2O (P less than 0.05). Thus our data indicate that increases in portal venous pressure to 34.4 +/- 9.0 cmH2O cause intestinal lymph flow to increase primarily because of increases in the effective PL.

Intra-abdominal fluid volume and hydrostatic pressure were elevated by positive pressure infusion of Tyrode solution into the peritoneal cavity of anesthetized dogs. The compliance of the peritoneal cavity fell from 10.8 to 0.56 ml X mmHg-1 X kg-1 of body wt as intra-abdominal pressure increased from 0 to 40 mmHg. Intrathoracic pressure also increased as elevated peritoneal pressure caused diaphragmatic bulging. Cardiac output and stroke volume were reduced by 36% after an intra-abdominal pressure rise of 40 mmHg; in contrast, heart rate did not change. Flow in the celiac, superior mesenteric, and renal arteries was reduced by 42, 61, and 70%, respectively. Pressure in the femoral vein increased to 46 mmHg, while flow in the femoral artery decreased by 65%. Whole-body O2 consuxmption, pH, and arterial PO2 decreased as intra-abdominal pressure rose. The peritoneal cavity, with its high initial compliance, affords the body an ideal location for the temporary accumulation of small to moderate volumes of fluid during episodes of increased vascular pressure or permeability. The marked alterations in the hemodynamic properties of the cardiovascular system are indicative of the physiological changes that occur when intra-abdominal fluid accumulation becomes excessive and peritoneal pressure rises to high levels.

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.