A Study on Mechanism of Ascites Absorption with Special Reference to Cirrhotic Ascites

Abstract

A study was made on tetrachloride induced-cirrhotic rats with ascites as well as on normal rats to study the mechanism of ascites absorption from the peritoneal cavity.
1) In normal rats, parasternal lympf vessels and a vessel along the right phrenic nerve were clearly demonstrated in X-ray films following peritoneal injection of Thorotrast. In the rats in which the parasternal lymph vessels had been ligated, the appearance in serum of radioactive goldcolloids infused into the peritoneal cavity, was significantly delayed. These findings suggest that the parasternal lymph vessels are the main route for the lymphatic drainage from the peritoneal cavity to the greater circulation.
2) In the X-ray study of the cirrhotic rats with ascites, the thoracic duct was clearly visualized after intraperitoneal injection of Thorotrast in addition to the mediastinal lymph vessels, suggesting that the thoracic duct plays also an important role in the drainage of ascites in cirrhosis.
3) The appearance in serum and the uptake into the liver, kidney and spleen, of radioactive gold colloids, infused into the peritoneal cavity, were greater in cirrhotic rats than in normal rats.
4) The thoracic lymph volume and the appearance in the thoracic lymph of radioactive gold colloids or ¹³¹I-albumin, infused into the peritoneal cavity, were greater in cirrhotic rats with ascites than in normal rats.
5) The study with electoron microscopy revealed that the gold colloid particles, infused into the peritoneal cavity, were pinocytosed into the mesothelial cells and drained into the lymph vessels of the diaphragm within five minutes of infusion.
In cirrhotic rats with ascites, the mesothelial cells of the peritoneum appeared to be thicker and have more pinocytic vesicles.
These findings seem to indicate that, in cirrhotic rats with ascites, the peritoneum becomes more active in the removal of colloid particles in ascites and their carrier ascitic fluid.