Intraperitoneal pressure in formation and reabsorption of ascites in cats.

The rate of ascites formation or reabsorption was recorded in anesthetized cats using the technique of intraperitoneal plethysmography. Hepatic venous pressure was increased using an extracorporeal circuit to drain effluent blood from the liver. When the intraperitoneal pressure was set to zero, elevation of hepatic venous pressure increased portal pressure and produced a constant rate of ascites formation. However, equivalent increments of portal pressure without elevation of hepatic venous pressure did not cause ascites formation, indicating that the liver was the source of ascites when hepatic venous pressure was increased. The rate of ascites formation was proportional to hepatic venous pressure, but elevation of the intraperitoneal pressure reduced the transsinusoidal pressure gradient responsible for fluid filtration from the liver. Although this reduced the rate of ascites formation, a secondary effect partly opposed this reduction in filtration rate. From this study and from previous work, there are now quantitative data showing that the intraperitoneal pressure is an important factor which accelerates the rate of reabsorption and decreases the rate of formation of ascites to bring these processes into equilibrium.