Ascitic Fluid Production Research Articles

Ascites production in 17 mouse strains.

SummaryMouse strains vary in their production of ascitic fluid. Intraperitoneal injections of heat-killed Staphylococcus aureus-incomplete Freund's adjuvant mixtures induce early development of ascites. Yield of ascitic fluid may be greater with adjuvant alone but production is often delayed. Yield in individual mice may be very large. High late yield for BALB/cAnN mice receiving only adjuvant are associated with occurrence of plasma cell tumors.

Production in Mice of Ascitic Fluid Containing Antibodies Induced by Staphylococcus- or Salmonella- Adjuvant Mixtures

Summary Substantial quantities of ascitic fluid containing antibodies were obtained from virtually 100% of mice injected with antigenic materials derived from either Staphylococcus aureus 18, Staphylococcus aureus 2 or Salmonella enteriditis mixed with incomplete Freund's adjuvant. High yields of ascitic fluid were elicited with 2–3 intraperitoneal inoculations of 0.4–0.5 ml of antigen-adjuvant mixtures administered at 3–7 day intervals. “Booster” doses caused a further increase in yield. Production of ascitic fluid, however, was not continuous for all the injected mice and for a 4-month period actual yield was 12–15 ml/mouse for persistent producers and 4–6 ml/mouse for the total number inoculated. Increased ascitic fluid yield was also obtained by concomitant employment of antigen-adjuvant mixtures and enzymes, hyaluronidase or trypsin. Ascites was elicited in four different strains of mice with production of substantial amounts of ascitic fluid comparable for all strains except A/HeN where yield was low. Heavier mice, weighing in excess of 20 g were found to be less susceptible to the lethal effects of inoculations with antigen-adjuvant mixtures. Studies of gross and microscopic pathology of ascitic mice revealed the presence of large numbers of plasma cells in peritoneal granulomas and in peripheral lymph nodes. Employing S. aureus 18-paraffin oil adjuvant mixtures, agglutinin titers showed an early rise (1:500–1:1000) which persisted at constant high levels for a period of 4–5 months. Comparable titers were found for the limited number of serums tested. Changes made in treatment of antigenic materials or in immunization schedules did not appreciably affect agglutinin titer. S. enteriditis protective antibodies were demonstrated in both immune mouse serum and immune mouse ascitic fluid. “Immune” ascitic fluid (0.005 ml) or immune serum (0.01 ml) afforded 50% protection to mice against S. enteriditis challenge. Injections of immunizing mixtures of S. enteriditis and paraffin oil by different routes produced comparable titers of agglutinating antibodies in the ascitic fluid. Total and differential counts of leukocytes in ascitic fluid typically revealed early in ascites 54,000 leukocytes/cu mm of which only 40% were mononuclears, whereas fluid obtained in late ascites contained 16,500 cells of which more than 90% were mononuclears. Eighty-eight per cent of the ascitic fluids measured for specific gravity fell in the range of 1.010 to 1.040. The γ-globulin average level for ascitic fluid was 0.86 g/100 ml and constituted on the average about 22% of the total protein. Protein levels for ascitic fluid were about 70% that for serum. Ascitic fluid was demonstrated to be a potential source of protective and agglutinating antibodies, viable leukocytes and γ-globulin. Induction of ascites in mice was accompanied by plasma cell proliferation in abdominal lymph nodes and granulomas.

PROTEIN METABOLISM AND EXCHANGE AS INFLUENCED BY CONSTRICTION OF THE VENA CAVA

Further studies of ascitic fluid production and related factors in dogs with constriction of the vena cava above the diaphragm are reported. Whole dog plasma given intravenously to such animals produces a rise in circulating plasma protein to normal levels, but increases the output of ascitic fluid with a loss of protein via the ascites equivalent to 72, 76, and 65 per cent respectively, of the injected protein. Forced ingestion of water in excess of the test animal's normal needs and desires produces no significant changes in the circulating plasma protein level or in ascitic fluid production. Amino acid growth mixtures given intravenously in distilled water cause weight loss, elevation of circulating plasma proteins, a slightly negative nitrogen balance, but no ascitic fluid production. Amino acid growth mixtures given intravenously in normal saline cause depression of the circulating plasma proteins, negative nitrogen balance, and significant ascitic fluid production. Ascitic fluid given intravenously to the test animals causes a marked depression of circulating plasma proteins, a marked increase in ascitic fluid production containing the equivalent of 116 and 98 per cent of the injected protein, and a negative nitrogen balance. Ascitic fluid given orally produces a marked depression of circulating plasma proteins, and a marked increase in ascitic fluid secretion, containing the equivalent of 66, 66, and 54 per cent respectively, of the ingested protein. Sodium chloride is a dominant factor in some of these experiments where abundant ascites production is recorded. Protein levels and intake are important, but take second place to sodium. Ascitic fluids show electrophoretic patterns which are almost identical to the plasma patterns. The A/G ratios are often equal in ascitic fluid and plasma, sometimes even lower in the ascitic fluid. This emphasizes the ease with which globulins pass cell or other membrane barriers in these experiments.

Failure of the Peritoneal-Button Operation for Ascites

THE surgical treatment of patients with recurrent massive ascites that requires frequent abdominal paracentesis has long been a challenging problem. Operative procedures designed to remedy the defect have carried an appreciable mortality, particularly in patients with portal obstruction due to hepatic cirrhosis who develop ascites relatively late in the course of the disease. Such procedures fall into several well defined groups. Some of these are designed merely to rid the patient of an oppressive volume of fluid; others attempt to eliminate factors in the production of ascitic fluid, and still others attempt to improve the body economy by returning water, . . .