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PubMed1988

[Pharmacokinetics of cefotaxime in cirrhotic patients with or without ascites].

Pharmacokinetic values of cefotaxime were measured in 12 cirrhotic male patients (6 without ascites and 6 with ascites) after intravenous injection of a single 2 gram dose of the antibiotic. In patients without ascites elimination of the drug was about the same as in normal subjects or control patients, although clearance was increased. In patients with ascites, the drug elimination half-life was significantly more prolonged (7.5 +/- 3.9 h versus 1.3 +/- 0.4 h, P less than 0.01) and the drug clearance was significantly lower (193.6 +/- 92.4 ml/min versus 475.8 +/- 152.2 ml/min, P less than 0.01) than in the other group. The accumulation of cefotaxime in these patients produced concentration in the ascites fluid that were above the critical therapeutic values for about 20 hours.

Ascites↗
PubMed1988

[Clinical and pharmacokinetic study of ceftriaxone in the treatment of 14 episodes of ascitic fluid infection].

A clinical study and dosages of ceftriaxone were performed during the treatment of 14 ascitic fluid infections. Fourteen cases of ascitic fluid infection were treated with ceftriaxone at doses of 2 grams daily. The isolation of the causative organisms was obtained in 11 out of 14 cases by systematic culture of the ascitic fluid in hemoculture bottles with aerobic and anaerobic medium. Of 11 evaluable infectious episodes ten were cured. Ceftriaxone diffuses rapidly in the ascitic fluid because, within the first hour; mean concentrations were already of 18.6 micrograms/ml largely exceeding the usual MIC for these organisms. A good tolerance for the drug, the well spaced rythm of infections preventing unnecessary parenteral treatment in cirrhotic patients, and its effectiveness against Enterobacteriaceae justify its choice in the treatment of ascitic fluid infections with sensitive organism.

Aged↗
PubMed1988

[Vaseline-peptone mixture as a stimulant of ascites formation in mouse hybridoma carriers].

A preliminary injection of vaseline oil with 3% of peptone in a dose of 0.5 ml induced ascitic tumors with a high taking rate in mice used as recipients of hybridomas. The dependence of the amount of ascitic fluid produced in such animals and the content of monoclonal antibodies on the time of the preliminary injection of the above-mentioned mixture, the number of cells introduced into the recipient animal, and the time of ascites collection has been studied. The optimal scheme of obtaining ascites with the use of the proposed mixture is presented. The comparison of the mixture with other stimulants of ascites production has been made.

Animals↗
PubMed1987

Beta 2-microglobulin in liver cirrhosis: study of a local synthesis in ascitic fluid.

Beta 2-microglobulin determinations in ascitic fluid (A) and serum (S) collected on the same day, were performed in 24 patients suffering from alcoholic liver cirrhosis. Ascitic beta 2-m concentration varied from 0.4 to 4.6 mg/l for patients with a normal renal function. Much higher values were found in patients with chronic renal failure. No correlation could be established between ascitic beta 2-m level and the clinical evolution of the cirrhosis. Comparative measurements of beta 2-m S/A ratio and albumin, transferrin, total protein S/A ratios suggests a local synthesis of beta 2-m in ascitic fluid. This is confirmed by an immuno-cytochemical technique which reveals the localisation of beta 2-m in the cytoplasm of peritoneal cells. The presence of beta 2-m in ascitic fluid seems to be related to an ultrafiltration across the peritoneal membrane as well as a local polyclonal activation of the immune system.

Adult↗
PubMed1988

Pericardial effusion and left ventricular dysfunction associated with ascites secondary to hepatic cirrhosis.

Fluid retention in decompensated hepatic cirrhosis is frequently accompanied by edema, ascites, and hydrothorax. Whether pericardial effusion occurs in such patients has not been studied. Twenty-seven consecutively hospitalized patients with ascites secondary to alcoholic cirrhosis of the liver were studied, and 28 control subjects were studied with the use of an echocardiographic method to detect pericardial effusion and to evaluate their left ventricular (LV) function. Seventeen patients (63%) and three control subjects (11%) showed pericardial effusion. The prevalence of pericardial effusion in the patients was significantly greater than in the control subjects (chi 2 = 10.6). Although the mean values of the echocardiographic measurements of LV function of the patients and the control subjects did not differ significantly, the individual values of the patients varied considerably. Among the patients, six patients (27%) had LV dysfunction, 14 patients (64%) had normal values, and two patients (9%) had values suggestive of hypercontractility of the left ventricle. Furthermore, abnormal systolic motions of the mitral valve and/or septum were noted in eight patients (30%) but in none of the control subjects. Six patients with pericardial effusion on initial examination were evaluated after the resolution of their ascites; pericardial effusion disappeared in two patients, diminished in two others, and remained unchanged in two patients. Resolution of ascites was also associated with normalization of the systolic motion of the mitral valve and septum. It was concluded that pericardial effusion is common in patients with ascites secondary to alcoholic hepatic cirrhosis and that its presence is probably related to fluid retention.

Adult↗
PubMed1987

Preliminary characterization of the procoagulant material in human ascites.

Disseminated intravascular coagulation invariably accompanies placement of peritoneovenous (LeVeen) shunts, which suggests that ascitic fluid contains procoagulant material capable of activating blood coagulation. In this study, we identified thrombogenic activity in human ascites and the hemostatic pathway by which it acts. Peritoneal fluid was removed percutaneously from patients with ascites due to various causes. Four fractions were prepared by centrifugation: cells, a low-speed, cell-free fluid, a high-speed supernatant, and the precipitate from the high-speed centrifugation. Cellular fractions from all ascitic fluids shortened a one-stage clotting time of normal pooled plasma by 68% in comparison with saline solution and endotoxin controls. Similarly, the cell-free fluids also shortened the clotting time of normal pooled plasma by 41%. The cellular and cell-free fractions shortened the clotting time of factor VIII-deficient plasma but failed to demonstrate procoagulant activity in factor VII-deficient plasma. These fractions had no effect on platelet aggregation or the platelet release reaction. The high-speed precipitate was dissociated by ethylenediaminetetra-acetate (EDTA) into fluid phase and precipitate, both of which demonstrated procoagulant activity. Furthermore, high-speed precipitate contained protein, phospholipid, and sterol in proportions similar to those of plasma membranes and contained membrane-bound vesicles as identified by means of electron microscopy. This material could be rendered inactive by heating to 100 degrees C for 2 minutes or by incubation with phospholipase C for 15 minutes. Finally, the ability of the high-speed precipitate to shorten the clotting time was prevented by preincubation with a monoclonal antibody, which is known to inhibit the procoagulant activity of human tissue factor. We suggest that several entities contribute to the procoagulant properties of human ascites, with procoagulant material deriving at least in part from peritoneal cells. The sedimentable procoagulant factor appears to be associated with cellular membranes or membrane fragments and is thromboplastin-like in its chemical composition, immunoreactivity, and substrate specificity.

Adult↗
PubMed1987

Dialytic ultrafiltration by hemofilter in treatment of patients with refractory ascites and renal insufficiency.

Six cirrhotic patients with intractable ascites had coexisting renal insufficiency. Dialytic ultrafiltration of ascitic fluid by hemofilter was attempted in these patients for symptomatic relief. The hemofilter removes fluid and substances with a molecular weight less than 50,000 daltons and the concentrated ascitic fluid was reinfused into the peritoneal cavity after ultrafiltration. A transient increase in urine output (p less than 0.01), urinary sodium excretion (p less than 0.01), and endogenous creatinine clearance (p less than 0.02) was noted and the plasma creatinine levels had remained stable for more than 4 months after the procedure. Our study suggests that dialytic ultrafiltration of ascites by hemofilter is a safe method in the management of patients with refractory ascites and renal insufficiency.

Adult↗
PubMed1987

Chylous ascites caused by constrictive pericarditis.

Chylous ascites is an uncommon clinical entity associated with lymphatic obstruction usually caused by underlying malignancy. The authors describe a patient with chylous ascites caused by constrictive pericarditis in the absence of mechanical lymphatic obstruction. Pathophysiological mechanisms for the development of chylous ascites in constrictive pericarditis include augmented lymph production and high impedance to lymph drainage caused by central venous hypertension. After pericardiectomy, the patient's ascites and edema resolved. Constrictive pericarditis should be considered a rare but potentially curable cause of chylous ascites.

Chylous Ascites↗
PubMed1986

Longstanding intractable ascites as the initial and predominant manifestation of systemic lupus erythematosus.

Peritoneal involvement is quite common in systemic lupus erythematosus (SLE). However, significant ascites as the predominant manisfestations of SLE is extremely rare, and very few cases have been reported. We describe a patient with SLE whose disease first manifested as longstanding, painless and intractable ascites. The ascites preceded the diagnosis of SLE by 3 years. The diagnosis of SLE should be considered in patients with the so called "idiopathic" ascites. Once diagnosed, the ascites seem to respond promptly to corticosteroids, however, prior to their administration other potential causes, especially infections and malignancy, should be ruled out.

Adult↗
PubMed1986

[Conditions for forming ascitic tumors in hybridoma cultivation in vivo].

The conditions of the formation of ascitic cells in BALB/c mice injected with hybridoma cells were studied. All the hybridomas under study, producing monoclonal antibodies to viral antigens, induced the formation of ascitic tumors when introduced into the abdominal cavity of BALB/c mice pretreated with sensitizing agents. In the mice pretreated with pristane hybridoma cells took at a rate of 43-80% and in the mice pretreated with Freund's complete adjuvant, 31-70%. Angara oil and perfume oil, as well as Bayol F, were less effective. The time of the formation of ascites was inversely proportional to the dose of the injected cells, while the volume of ascitic fluid depended rather on the type of hybridoma and not on the dose of the injected cells. The study showed that the use of physiological saline or culture medium without serum for washing the abdominal cavity of mice after withdrawing ascites permitted the additional collection of 2.6-13.7 million hybrid cells, as well as a considerable amount of immunoglobulins.

Animals↗
PubMed1985

Amino acid patterns in the plasma and ascitic fluid of cirrhotic patients.

Amino acid levels were measured in the plasma and ascitic fluid of 13 alcoholic patients with liver cirrhosis and of 14 normal controls. The plasma aromatic amino acids of the alcoholic patients were not statistically different from those of the control subjects, whereas the levels of branched-chain amino acids were reduced (P less than 0.05). The values for the ratio of the muscle/liver metabolized amino acids (valine + isoleucine + leucine)/(phenylalanine + tyrosine + methionine) were statistically lower in the cirrhotic patients both in plasma and ascitic fluid (P less than 0.05). The amino acid levels in the ascitic fluid of the cirrhotic patients were slightly lower than those in the plasma of the same patients and the values for the muscle/liver metabolized amino acid ratio were similar in plasma and ascitic fluid. Aspartic acid, glutamic acid and glycine levels were higher among the cirrhotic patients (P less than 0.05). Cirrhotic patients present an alteration in amino acid metabolism which creates a different amino acid pattern in both plasma and ascitic fluid. The significance of the proposed ratio and its possible relation to hepatic failure are discussed.

Adolescent↗
PubMed1978

Differential immunosuppressive effects of ascites fluid from mastocytoma-bearing mice on primary vs secondary immunocyte responses.

The effects of immunosuppressive ascites fluids from mastocytoma-bearing mice on the primary vs secondary immune response to sheep red blood cells (SRBC) was examined. Injection of mice with ascites fluid from tumor-bearing mice markedly depressed the primary immune response of normal syngeneic mice challenged with SRBC. However, there was a preferential depression of the 19S IgM antibody response as compared with the 7S IgG response. Injection of ascites fluid shortly before secondary immunization of mice with SRBC also resulted in depressed IgM PFC responses but only a slight to moderate depression of IgG PFC. Treatment of mice with the ascites fluid before primary immunization had little if any effect on the secondary IgG PFC response, although the IgM response was moderately depressed. These results indicate that the immunosuppressive factor(s) present in the ascites fluid of mastocytoma-bearing mice has a differential effect on distinct classes of immunocytes. Those immunocytes or their precursors involved in formation of low efficiency 7S IgG antibody are more resistant to immunodepression. Such differences appear due to different sensitivities of cells involved in the immune response system.

Animals↗
PubMed1981

[Diagnostic value of laboratory examination of ascites fluid (author's transl)].

Measurement of lactate dehydrogenase (LDH), glucose and protein was performed in ascites fluid of 44 patients in addition to bacteriological and cytological examinations. In patients with cirrhosis of the liver protein content of ascites was low, LDH normal, and the ascites/serum ratio of glucose concentration was higher than 1. These values were statistically significant different from the values in patients with tumorous or inflammatory disease of the peritoneum - protein and LDH in the ascites fluid being high and the ascites/serum ratio of glucose concentration being below 1. Cirrhosis however and tumors of the liver could not be differentiated by this method. Ascites from patients with cardiac failure had high protein content. In patients with liver cirrhosis high concentrations of protein in ascitic fluid may mean possibly a better survival time.

Adolescent↗
PubMed1980

Isolation of an inhibitor of type II interferon induction from tumor ascitic fluids.

A low-molecular-weight fraction (M.W. approximately 700) that specifically impairs the induction of type II interferon in mice by purified protein derivative of tuberculin or OK-432 was isolated from the cell-free ascitic fluid of mice bearing Ehrlich ascites carcinoma. Purification was achieved by ultrafiltration and gel filtration. The inhibitory activity of the isolated fraction was 10 times greater than that of the unfractionated starting material in the impairment of type II interferon induction. The significant inhibition was observed even when 0.2 ml of the 10,000-fold dilution of the fraction, which was previously adjusted to 0.25 A unit at 290 nm absorption, was once treated i.p. in normal mice 48 hr before challenge of type II interferon inducers. This fraction was stable to heating at 56 degrees for 60 min. The active component, however, did not affect the in vivo induction of type I interferon by polyriboinosinic-polyribocytidylic acid or tilorone-HCl. In parallel experiments, an identical low-molecular-weight fraction that impairs the type II interferon induction in mice was isolated from the ascitic fluids of rats bearing AH-100B ascites tumor and from a human hepatoma case with advanced cancer metastatic to the peritoneal cavity. However, nontumorous ascitic fluids obtained from adjuvant-stimulated mice and a human liver cirrhosis case did not contain any such inhibitory activity.

Animals↗
PubMed1978

Renal sodium retention and ascites formation in dogs with experimental cirrhosis but without portal hypertension or increased splanchnic vascular capacity.

Renal handling of sodium was studied in five dogs where an end-to-side portacaval fistula was constructed prior to the induction of cirrhosis with DMN. Such a model permits the effects of cirrhosis to be studied separately from the consequences of portal hypertension. Three control animals without cirrhosis maintained normal liver and kidney function and remained in sodium balance for as long as 8 weeks following surgery. In the five cirrhotic dogs, urinary sodium retention preceded ascites formation and was independent of hyperaldosteronism, hypoalbuminemia, hepatic ischemia, or decreased renal perfusion. Portal venous pressure remained normal in all cirrhotic dogs, and the splanchnic area remained free of venous collaterals. Plasma volume expansion also preceded ascites formation, and this variable increased by 8.4% (p less than 0.05) following 6 days of sodium retention. These temporal relationships between sodium retention, expanded plasma volume, and ascites formation are similar to those observed in ordinary cirrhotic dogs previously studied in this laboratory. Total plasma volume increased by 13.2% (p less than 0.05) when measured during the ascitic phase of cirrhosis. However, when the splanchnic and nonsplanchnic ("effective") components of plasma volume were measured by an exclusion technique, the ratio of these components to total plasma volume was not different from that observed in normal dogs. Thus no preferential consignment of retained salt and water had occurred. We conclude that urinary sodium retention in cirrhotic dogs occurs independently of portal hypertension or augmented splanchnic vascular capacity and is associated with expansion of the effective plasma volume, even though ascites is present.

Abdomen↗
PubMed1983

Improved efficiency of hybridoma ascites production by intrasplenic inoculation in mice.

Intrasplenic inoculation of small numbers (10(4)) of antibody-producing hybridoma cells into unprimed BALB/c mice resulted in high-titered ascites. By intrasplenic injection, the low number of cells needed to produce ascites was 2-3 logs fewer than that required by ip inoculation. Hybridoma cells suspended in the ascitic fluid could be reestablished in vitro. Furthermore, cells obtained directly from individual, cloned colonies or from previously frozen samples also resulted in high-titered ascites, if the cells were inoculated intrasplenically. This method reduces time and expense required to grow large numbers of hybridoma cells for ip-derived ascites production and allows ready recovery of frequently unstable frozen-thawed cells.

Animals↗
PubMed1984

Changes in lipoprotein lipase activity (LPLA) in tumor cells and tissues in mice bearing Ehrlich ascites tumor.

Lipid content and lipoprotein lipase activity (LPLA) of serum and various tissues of mice bearing Ehrlich ascites tumor have been studied. The growing tumor caused hyperlipidemia, depletion of adipose tissue, a slight increase of heart lipid content, lipid accretion in the tumor cells and a relative increase of free fatty acids and cholesterol in the ascites fluid. LPLA of the post-heparin plasma was higher in tumorous than in control mice. Tumor growth led to a marked decline of LPLA in the adipose tissue and an elevation in the heart. It declined slightly in the older tumor cells and increased in the ascites plasma of the same. It has been concluded that: a) decline in adipose tissue LPLA may play an important part in the development of hyperlipidemia and loss of body fat; b) increase of the heart LPLA proves insufficient for elimination of the piled up blood lipids during progression; c) LPLA in the ascites fluid may favour the hydrolysis of triglycerides entering the ascites fluid, which might account at least in part for the fatty acids made available to the tumor; d) LPLA detected in the tumor cells might also facilitate the assimilation of lipids by the tumor cells.

Adipose Tissue↗
PubMed1983

Antitumor activity of macrophages grown in tumorous ascitic fluid.

Peritoneal macrophages from mice injected with glycogen proliferated in vitro in the presence of cell-free tumorous ascites. DNA synthesis of macrophages was also induced by ascitic fluid, but did not occur in the absence of the fluid. However, macrophage growth was inhibited at a higher concentration of ascitic fluid (greater than 20%). The growth stimulating activity of this fluid was stable on heat treatment. The adherent cultured cells that proliferated were typical macrophages, as indicated by nonspecific esterase staining, pinocytosis and phagocytosis. These macrophages showed cytolytic activity against a murine tumor in the presence of wheat germ agglutinin. However, their cytotoxicity with antitumor antibody decreased during the culture period. These results indicate that tumorous ascitic fluid contains a macrophage growth factor(s) and that macrophages cultured with, and induced to proliferate by, ascitic fluid can kill tumor cells in cooperation with lectin but not antibody.

Animals↗