Lymphatic absorption from the peritoneal cavity: Regulation of patency of mesothelial stomata

Absorption of fluid from the peritoneal cavity is carried out by terminal lymphatics, called lacunae, located in the diaphragm. Lacunae communicate with the peritoneal cavity via stomatal openings between mesothelial cells that lead into channels formed by juxtaposed processes of mesothelial and lacunar endothelial cells. We examined the patency of stomata under conditions of drug-induced relaxation or contraction of the diaphragm, increased intraabdominal pressure, and experimental ascites caused by intraperitoneal infection with Toxoplasma gondii. We observed numerous patent stomata when the diaphragm is relaxed and when intraabdominal pressure is raised. When the diaphragm is contracted we observed either few of no patent stomata. Ascites accompanying peritoneal parasitic infection resulted in 'hypertrophy' of mesothelial cells and fewer patent stomata. We then examined the means for regulating the patency of stomata and the conformation of endothelial flaps that extend across the lumen of channels. Using the technique of decoration of actin with the S1 subfragment of myosin, we identified numerous actin filaments in the cytoplasm of mesothelial and endothelial cells that border stomata and form channels. Treatment in situ of the diaphragm with cytochalasin D resulted in pronounced deformation of mesothelial cells overlying lymphatic lacunae and endothelial cells that line channels. The deformation was reversed after cytochalasin D was washed away with n-saline. Our findings indicate that the patency of mesothelial stomata can vary in response to changing conditions in the peritoneal cavity. They also indicate that maintenance of the normal conformation of stomata and channels and perhaps control of the patency of stomata as well rely upon actin components in the cytoplasm of mesothelial and endothelial cells.