Basic determinants of epicardial transudation.

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.

Regulation of microvascular filtration in the myocardium by interstitial fluid pressure.

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.

Renal lymphatic function following venous pressure elevation.

The renal lymphatic system plays an important role in removing excess fluid from the kidneys. Unfortunately, the factors influencing lymphatic flow are difficult to measure. We used a simple model to represent renal lymphatics as a single pressure source (PL) pushing lymph through a single resistance (RL). In anesthetized dogs, we cannulated renal lymphatics and measured lymph flow rate (QL) as we varied pressure (PO) at the outflow end of the lymphatics. There was no significant change in QL as we increased PO from -5 to 0 cm H2O. In other words, there was a plateau in the QL vs. PO relationship. At higher PO's, QL decreased linearly with increases in PO. From this linear relationship, we calculated RL as -delta PO/ delta QL and we took PL as the PO at which QL = 0 microliter/min. At baseline, RL = 0.34 +/- 0.14 (SD) cm H2O.min/microliter and PL = 8.2 +/- 4.4 cm H2O. When we increased renal venous pressure (PV) from baseline (3.5 +/- 3.0 cm H2O), the plateau in the QL vs. PO relationship extended to higher PO's, RL decreased, and PL increased. Renal interstitial fluid volume and interstitial pressure increased following elevation of PV. The extension of the QL vs. PO plateau with increasing PV suggests that renal interstitial pressure may partially collapse intrarenal collecting lymphatics which may compromise lymph flow.

Presumptive, iatrogenic gastric outflow obstruction associated with prior gastric surgery.

Iatrogenic gastric outflow obstruction in two dogs appeared to be caused by prior gastric surgery. The obstructions were believed to be anatomical rather than functional based on endoscopic examinations. Initially, the dogs had been evaluated and each had received two abdominal surgeries because of gastrointestinal bleeding, vomiting, or both. Eventually, both dogs were euthanized due to complications arising after attempted surgical correction of the iatrogenic obstructions. While gastric surgery commonly is performed, it seldom is considered to be a potentially harmful procedure. However, as these cases demonstrate, the decision to perform a gastrotomy must be weighed against possible risks and complications. Iatrogenic gastric outflow obstruction associated with surgery may be prevented by minimizing tissue inversion into the gastric lumen when surgery is performed near the pyloric outflow tract. Additionally, when large lesions near the pylorus are resected surgically, preservation of the continuity of the outflow tract is necessary.

Myocardial edema and compromised left ventricular function attributable to dirofilariasis and cardiopulmonary bypass in dogs.

We investigated the relation between left ventricular dysfunction and myocardial edema in dogs with heartworm (Dirofilaria immitis) infection that were undergoing cardiopulmonary bypass. Dogs with and without D immitis were anesthetized by continuous thiopental infusion and were mechanically ventilated. Sonomicrometry crystals were placed on the long and short axes of the left ventricle, and a Millar pressure transducer was placed in the left ventricular chamber. Pressure-volume loops were digitized and continuously recorded. Dogs with and without D immitis were placed on standard hypothermic cardiopulmonary bypass, with 1 hour of aortic cross-clamp. Wet-to-dry weight ratio corrected for residual blood volume was used to quantitate the volume of myocardial edema. Preload recruitable stroke work was used as a preload-independent index of systolic function. Tau, the isovolumic relaxation time constant, was determined to assess diastolic relaxation. Dogs with D immitis had increased baseline myocardial wet-to-dry weight ratio. After cardiopulmonary bypass, myocardial edema increased in all dogs. Acute edema attributable to cardiopulmonary bypass decreased preload recruitable stroke work in all dogs of both groups, and dogs with D immitis could not be weaned from cardiopulmonary bypass. Myocardial edema increased diastolic relaxation times (tau) in dogs with and without D immitis. We conclude that cardiopulmonary bypass and heartworm infection induce myocardial edema. This edema compromises left ventricular systolic and diastolic function making D immitis an important confounding factor in weaning dogs from cardiopulmonary bypass.