Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ASCITES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed1979

Ascites tumors in CBA mice. Characterization of two new tumors, a carcinoma and a sarcoma in solid and ascites form, with regard to cell surface properties and transplantability.

Two ascites tumors in syngeneic CBA mice are described, viz., MCB 21-AA and MCB 31-AA, with their solid progenitors: A sarcoma (MCB 21-SS) and a squamous cell carcinoma (MCB 31-SC), induced by gastric feeding of 20-methylcholanthrene. The ascites tumor cells have certain characteristics in common, which they do not share with either cells from the solid tumors or even with cells from solid ascites tumors (-21-AS and -31-AS=ascites tumor transplanted s.c.). Presumably some of these differences, for instance, in PAS stainability, electrophoretic mobility and lectin agglutinability, are due to enzyme treatment required to bring solid tumors into suspension. Between the two ascites tumors there are certain differences in cell size, aggregability, and growth rate. They are similar, however, in requiring large cell doses for transplantation in syngeneic animals, which is also true for the solid (SS and SC) tumors. MCB 21 and -AA even required fewer cells for transplantation in allogeneic A mice than in syngeneic CBA mice. MCB 31-AA is also allotransplantable. The pattern of spread, after i.v. cell injection, is almost exclusively to the lungs for all tumor lines.

Animals↗
PubMed1994

Ascites apheresis, concentration and reinfusion for the treatment of massive or refractory ascites in cirrhosis.

A new method for ascites recirculation, consisting of a cellulose diacetate filter to remove substances with molecular weight > or = 300,000, cell debris and bacteria, followed by the concentration of ascitic fluid prior to i.v. infusion, was used 24 times in 19 patients with cirrhosis and massive or refractory ascites. The amount of ascites removed was 7.67 +/- 0.49 l, which was reduced to 407 +/- 37 ml. The procedure took 367 +/- 22 min to complete. No statistically significant changes in liver function tests, coagulative parameters, platelet count or natremia were found. The activity of coagulation and fibrinolytic systems was further assessed in six patients. No changes suggesting an activation of intravascular coagulation and/or primary fibrinolysis were disclosed. An asymptomatic fall in mean arterial pressure (from 88.6 +/- 2.6 to 80.3 +/- 3.0 mmHg; p = 0.02) occurred after paracentesis and was still present 48 h after ascites reinfusion. Plasma renin activity significantly decreased at the end of the procedure, but was not associated with a proportional reduction of plasma aldosterone concentrations. Both variables returned to baseline values 48 h later. A significant increase in the glomerular filtration rate occurred just after the end of the procedure (from 50.4 +/- 9.1 to 73.1 +/- 23.5 ml/min; p < 0.05) and subsided 48 h later. In contrast, no significant changes in diuresis and renal sodium excretion were found. Complications due to volume overload and sepsis did not occur; in one case, spontaneous bacterial peritonitis developed 3 days after the procedure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Peritoneovenous shunting as compared with medical treatment in patients with alcoholic cirrhosis and massive ascites. Veterans Administration Cooperative Study on Treatment of Alcoholic Cirrhosis with Ascites.

The optimal management of severe ascites in patients with alcoholic cirrhosis has not been defined. in a 5 1/2-year study, we randomly assigned 299 men with alcoholic cirrhosis, who had persistent or recurrent severe ascites despite a standard medical regimen, to receive either intensive medical treatment or peritoneovenous (LeVeen) shunting. We identified three risk groups: Group 1 had normal or mildly abnormal results on liver-function tests, Group 2 had more severe liver dysfunction or previous complications, and Group 3 had severe prerenal azotemia without kidney disease. For the patients who received the medical treatment and those who received the surgical treatment combined, the median survival times were 1093 days in Group 1, 222 days in Group 2, and 37 days in Group 3 (P less than or equal to 0.01) for all comparisons). For all the groups combined, the median time to the resolution of ascites was 5.4 weeks for medical patients and 3.0 weeks for surgical patients (P less than 0.01). Within each risk group, mortality during the initial hospitalization and median long-term survival were similar among patients receiving either treatment. However, the median time to the recurrence of ascites in Group 1 was 4 months in medical patients, as compared with 18 months in surgical patients (P = 0.01); in Group 2 it was 3 months in medical patients as compared with 12 months in surgical patients (P = 0.04). The median duration of hospitalization was longer in medical patients than in surgical patients (6.1 vs. 2.4 weeks in Group 1 [P less than 0.001] and 5.0 vs. 3.1 weeks in Group 2 [P less than 0.01]). Group 3 was too small to permit a meaningful comparison. During the initial hospitalization, the incidence of infections, gastrointestinal bleeding, and encephalopathy was similar among the medical and surgical patients. We conclude that peritoneovenous shunting alleviated disabling ascites more rapidly than medical management. However, survival was closely related to the severity of the illness at the time of randomization and was not altered by shunting.

Ascites↗
PubMed1992

Blocking factors (soluble membrane receptors) for tumor necrosis factor and lymphotoxin detected in ascites and released in short-term cultures obtained from ascites and solid tumors in women with gynecologic malignancy.

Studies were conducted to identify and establish the cell and tissue source of blocking factors (BF), materials that inhibit the bioactivity of human TNF and LT in vitro. Ascites and samples of solid tumors were collected from women with various gynecologic malignancies. Supernatants were collected from cultures of tumor and ascites cells after 24, 48, and 72 h. Cell-free ascites (CFA) and culture supernatants were tested for their ability to block human recombinant TNF and LT-induced lysis of L929 cells in vitro. Levels of soluble forms of the 55- and 75-kDa TNF/LT receptors were measured by ELISA assay in the same samples. CFA and culture supernatants contained TNF/LT blocking factors and high levels of one or both soluble 55- and 75-kDa TNF/LT membrane receptors. Levels of BF bioactivity and receptors appeared rapidly, peaked at 24 h, and declined thereafter. Soluble TNF/LT receptors may be the active BF in these samples, and tumor tissues and ascitic cells may be a source of these receptors in the ascites fluid of these patients.

Ascites↗
PubMed1977

Chalone-like inhibition of Ehrlich ascites cell proliferation in vitro by an ultrafiltrate obtained from the ascitic fluid.

An aqueous ultrafiltrate (10 000-50 000 dalton) prepared from the cell-free ascitic fluid of mice bearing Ehrlich ascites tumour (EAT) in the plateau phase of growth (12-16 days after transplantation) was investigated with regard to its inhibitory effects on the proliferation of EAT cells in a 24-hr suspension culture. The following results were obtained: (1) The in vitro proliferation of cells obtained from the plateau phase of in vivo growth was reversibly inhibited. (2) The dose-response curves show a plateau with a maximum inhibition of about 50%, which suggests that not all cells can be affected. (3) Young cells (4-6 days after transplantation) were not inhibited. (4) Preincubation of plateau phase cells in the culture medium before treatment abolishes the inhibitory effect of the ultrafiltrate. This effect of preincubation is dependent on time and serum concentration. It provides the possibility to differentiate between true "chalone-like" and cytotoxic effects. (5) the inhibitory properties of the ultrafiltrate are destroyed by heating or trypsin treatment. (6) Extracts prepared in the same way from ascitic fluid of mice bearing lymphocytic leukemia L1210 do not inhibit the proliferation of EAT cells. Corresponding extracts from ascitic fluid of mice bearing myelocytic leukemia YM were found to be inhibitory; however, the inhibitory effect was also found on preincubated cells and is therefore considered to be due to an unspecific cytotoxicity. In conclusion, evidence was obtained for a factor from the ascitic fluid of mice bearing EAT, which prevents EAT cells from entering the proliferating state.

Animals↗
PubMed1985

[Surgical therapy of ascites--results of peritoneovenous drainage with the Hakim-Cordis ascites valve].

Peritoneo-venous shunting of ascites was performed in 16 patients using the Hakim-Cordis ascites valve system. After an average of 4.3 months four patients presented with closure of the valve or deconnection of the system that is to say, complications caused by the valve system. Early postoperative complications occurred in 7 patients; they usually can be avoided. Correct placement of the system has to be controlled intraoperatively by x-ray examination. If the ascites fluid contains much protein, repeated depressing and releasing of the antechamber has to be performed in order to avoid obstruction. The probability of diffuse intravascular coagulation (DIC) after valve placement can be predicted by measuring certain coagulation parameters preoperatively after intravenous infusion of ascites. We conclude, that because of high flow rate, easy placement of the small-sized catheter and up to now good clinical results the Hakim valve system offers an enrichment of the therapeutic methods in resistant ascites.

Ascites↗
PubMedDate not supplied

Ascitic fluid filtration and intravenous infusion versus total-volume paracentesis with infusion of plasma expander in cirrhosis with tense or intractable ascites.

BACKGROUND: Patients with cirrhotic ascites have low serum albumin levels, and paracentesis of ascitic fluid could compromise them further. AIM: We compared the therapeutic efficacy of ascitic fluid filtration and concentrate infusion (AFI) versus total-volume paracentesis (TVP) with colloid infusion in control of tense or intractable cirrhotic ascites. METHODS: Ten patients underwent AFI; their ascitic fluid was filtered repeatedly through hollow-fiber hemodialyzer, and the concentrate reinfused intravenously. In ten patients TVP was done with simultaneous intravenous colloid infusion. Follow-up was done weekly and the study terminated if the patient needed diuretics or developed complications. RESULTS: Pre-study parameters were similar in the two groups. In the AFI and TVP groups, the duration of procedure was median 12 hours and 5.5 hours; fluid removed by paracentesis was 10.2 L and 8.0 L, respectively; and fluid infused intravenously was 0.5 L [with mean (SD) protein content 5.7 (1.3) g/dl] and 1.1 L, respectively. Glomerular filtration rates were lower than normal in the two groups but did not change significantly with the procedure; body weight remained significantly lower up to week 3 and week 2, respectively. The study was terminated at median week 3 (range 1-8) and week 2 (1-4), respectively. Fever was an accompaniment of AFI and one patient developed peritonitis. CONCLUSION: Patients undergoing AFI remained diuretic-free longer; the procedure is cost-effective but needs to be further evaluated to minimize the side-effects.

Ascites↗
PubMed1990

Hydrocortisone protects cycloheximide-challenged mice pretreated with Ehrlich ascites tumour cells or with cell-free Ehrlich ascites tumour fluid.

The invariably fatal outcome following cycloheximide challenge of mice pretreated 24 h earlier with either 1 x 10(7) washed Ehrlich ascites tumour cells i.v. or with 0.2 ml of cell-free Ehrlich ascites tumour fluid i.v. was prevented by hydrocortisone treatment. However, glucocorticosteroids failed to prevent the fatal outcome of cycloheximide challenge in mice bearing 5-day-old Ehrlich ascites tumours. The results are interpreted as indicating that there is a steroid demand which must be met to ensure survival of cycloheximide-challenged mice pretreated with tumour cells or with cell-free tumour ascites fluid and that an additional and essential requirement for uninterrupted protein synthesis exists in the case of mice with established ascites tumours and challenged with cycloheximide.

Animals↗
PubMed1980

Reassociation of eukaryotic ribosomal subunits and polyamine concentration in Yoshida ascites hepatoma and Ehrlich ascites carcinoma cells during growth.

The activity on ribosome monomers of dissociation factor preparations obtained by high salt wash from ribosomes and from the post-ribosomal supernatant (cytosol) of Yoshida rat ascites hepatoma and Ehrlich mouse ascites carcinoma cells and from the liver of control and tumor-bearing animals has been determined at different periods of intraperitoneal tumor growth. The concentration of the polyamines spermine, spermidine and putrescine has also been measured under the same conditions. Results here reported show the presence of an association factor activity on subunit ribosomes at low Mg2+ concentrations in the post-ribosomal supernatant fractions of Yoshida ascites hepatoma and Ehrlich ascites carcinoma cells during tumor growth. An association factor activity also takes place in the ribosomal high salt wash extracts of Yoshida ascites cells at the terminal stages of tumor growth. Since an increase of spermidine to putrescine ratios occurs during tumor growth the changes in the rate of ribosome monomer dissociation into units here observed might be attributable, at least in part, to changes in polyamine concentrations under the conditions studied.

Animals↗
PubMed2001

Electrospray ionization mass spectrometry analysis of lysophospholipids in human ascitic fluids: comparison of the lysophospholipid contents in malignant vs nonmalignant ascitic fluids.

Lysophospholipids (lyso-PLs), including various glycerol-based and sphingosine-based lysophospholipids, play important roles in many biochemical, physiological, and pathological processes. The classical methods to analyze these lipids involve gas chromatography and/or high-performance liquid chromatography, which are time-consuming, cumbersome, and sometimes inaccurate due to the incomplete separation of closely related lipid species. We now describe the quantitative analysis of lyso-PLs in ascites samples from patients with ovarian cancer using electrospray ionization spectrometry. Three new classes of lyso-PL molecules are detected: alkyl-LPA, alkenyl-LPA, and methylated lysophosphatidylethanolamine. Importantly, the following lysophospholipid species are significantly increased in ascites from patients with ovarian cancer, compared to patients with nonmalignant diseases (e.g., liver failure): LPA (including acyl-, alkyl-, and alkenyl-LPA species), lysophosphatidylinositol, and sphingosylphosphorylcholine. Lysophosphorylcholine contents are also significantly different among ascitic fluids from the two groups of patients. However, the total phosphate content in ascites samples from patients with ovarian cancer is not significantly different compared to that from patients with nonmalignant disease.

Ascites↗
PubMedDate not supplied

Ascitic fluid analysis in the differentiation of spontaneous bacterial peritonitis from gastrointestinal tract perforation into ascitic fluid.

A review of patients with bacterial peritonitis and ascites revealed six patients with gastrointestinal tract perforation into their ascitic fluid and 33 episodes of spontaneous bacterial peritonitis in 32 patients. Signs and symptoms were not helpful in differentiating the two groups; however, ascitic fluid analysis was found to be useful. All patients with perforation peritonitis fulfilled at least two of the following criteria: ascitic fluid total protein greater than 1 gm per dl, glucose less than 50 mg per dl and lactate dehydrogenase greater than 225 mU per ml. In only two episodes of spontaneous bacterial peritonitis were two of the criteria fulfilled.

Ascitic Fluid↗
PubMed2005

Contribution of ascites to impaired gastric function and nutritional intake in patients with cirrhosis and ascites.

BACKGROUND & AIMS: Protein calorie malnutrition and weight loss are common among patients with cirrhosis and ascites. The cause of these symptoms is unclear, with several putative mechanisms proposed. The primary aims of this study were to compare gastric volumes and accommodation between patients with cirrhosis complicated by ascites and healthy controls, and to evaluate the effect of large-volume paracentesis in the patient group. METHODS: Patients with cirrhosis and ascites underwent assessment of gastric volumes as measured by single-photon emission computed tomography, gastric sensation assessed by a validated nutrient drink test, and a 3-day assessment of caloric intake before and after large-volume paracentesis. Age- and sex-adjusted linear regression models were used to compare gastric volumes and accommodation ratios between patients and healthy volunteers. Paired Wilcoxon rank-sum tests were used to compare gastric measures before and after paracentesis among the patient group. RESULTS: Fifteen patients (median age, 54 y) were compared with 112 healthy (age- and sex-matched) controls. Median postprandial gastric volumes (627 mL patients vs 721 healthy controls) and gastric accommodation were reduced significantly in patients compared with healthy controls (P = .02 and .006, respectively). After paracentesis: (1) fasting gastric volumes were increased (median 312 mL post- vs 241 mL pre-, P = .04), (2) patients tolerated ingestion of larger maximum volumes (median 964 mL post- vs 738 mL pre-, P = .04), and (3) caloric intake was increased (median 34% kcal post- vs 3110 kcal pre-, P = .005). CONCLUSIONS: Postprandial gastric volumes and accommodation ratios are reduced in patients with cirrhosis and ascites compared with healthy controls. In addition, large-volume paracentesis increases fasting gastric volumes, volumes ingested until maximal satiation, and caloric intake.

Aged↗
PubMed1994

Effect of a urease inhibitor and ceiling fans on ascites in broilers. 1. Environmental variability and incidence of ascites.

A low ventilation model to induce ascites was introduced and characterized. In addition, the effect of supplemental air mixing via ceiling fans (CF) and the feeding of a urease inhibitor (0, 125, and 250 ppm) on incidence of ascites were investigated. Twelve environmental chambers were utilized in the trial; six were fitted with CF. Each dietary treatment was replicated twice per CF treatment. One hundred and twenty day-old male commercial broilers were reared per chamber. Atmospheric O2, CO2, and NH3, temperature, and humidity, as well as weekly litter moisture and pH, were monitored. Chamber CO2 levels increased immediately then stabilized. Chamber NH3 levels increased between 2 to 4 wk of age and rapidly declined when ventilation rates were increased to 1 cfm per bird. The CF and dietary treatments had little effect on air or litter variables except for NH3. Supplementing the diet with urease inhibitor resulted in a greater than 50% reduction in cumulative mortality due to ascites and a slight reduction in weekly BW gains. The CF treatment had no effect on production variables such as weekly feed intake, gain, and feed to gain ratio, or survivability due to ascites.

Ammonia↗
PubMed1994

Effect of a urease inhibitor and ceiling fans on ascites in broilers. 2. Blood variables, ascites scores, and body and organ weights.

Restricted ventilation was used to experimentally induce ascites in commercial male broilers. The role of a dietary urease inhibitor (0, 125, and 250 ppm) and ceiling fans to reduce ascites was investigated. At 6 wk of age, birds were bled, euthanatized, weighed, scored for ascites, and heart, liver, and small intestine weights were obtained. Random samples were analyzed for intestinal ammonia. Blood samples were analyzed for blood gases, hemoglobin, red blood cell count, blood urea nitrogen, ammonia, and uric acid. Birds fed 125 and 250 ppm urease inhibitor were significantly (P < .001) lighter at 6 wk, when compared with controls. Urease inhibitor (125 and 250 ppm) significantly decreased large intestine ammonia. Urease inhibitor significantly increased small intestine (250 ppm) and liver weights (125 and 250 ppm), whereas urease inhibitor at 125 ppm decreased right ventricular heart weight. Urease inhibitor had no effect on ascites scores, blood gases, or blood ammonia, but hemoglobin, blood urea nitrogen, red blood cell count, and uric acid were significantly (P < .05) decreased by 125 ppm urease inhibitor.

Animals↗
PubMed1976

Characterization of dextran sulfate-treated ascites tumor cells and their repair by ascites fluid.

Exposure of Ehrlich ascites tumor cells to the polyanion dextran sulfate altered the permeability of the plasma membrane resulting in decreased glycolysis and respiration, enhanced permeability to Rb+ and adenosine 5'-triphosphate, and increased staining by erythrosin B. The inhibition of respiration was reversed by the addition of inorganic phosphate, whereas restoration of glycolysis required both inorganic phosphate and adenosine 5'-monophosphate. The membrane lesion was repaired by injection of dextran sulfate-treated cells into mice or by in vitro exposure to a heat-stable extract from ascites fluid. Reparied cells were no longer stained by erythrosin B and glycolyzed without added adenosine 5'-monophosphate. The time course of repaire was separable into a rapid initial repair of the membrane lesion followed by a slower recovery of the normal intracellular ionic composition. Both phases were insensitive to inhibitors of protein synthesis. The repair activity of ascites fluid was heat stable and was composed of both dialyzable and nondialyzable factors. Incubation of dextran sulfate-treated cells with ascites fluid restored Rb+ uptake and abolished the adenosine 5'-triphosphate-stimulated Ca2+ uptake.

Adenosine Monophosphate↗
PubMed1988

Fatal susceptibility to cycloheximide of mice bearing Ehrlich ascites tumours and of animals pretreated with cell-free Ehrlich ascites tumour fluid.

Soluble, but unidentified, factors in cell-free Ehrlich ascites tumour fluid induced, after a delay period, a fatal heparin- and ancrod-resistant susceptibility to a normally tolerated dose of cycloheximide. The evidence suggests that production of such factors is dependent upon interaction of tumour cells with the intravascular or the intraperitoneal compartment. The factors are considered likely also to play a crucial role in the similar heparin and ancrod-resistant fatalities which follow cycloheximide challenge of mice bearing established Ehrlich ascites tumours and in the deaths of mice challenged with cycloheximide 24 h after an intravenous injection of washed Ehrlich ascites tumour cells. These factors play no part in the heparin- and ancrod-preventable fatal syndrome following cycloheximide challenge either 2 h before or 2 h after intravenous injection of washed Ehrlich ascites tumour cells.

Ancrod↗
PubMed1976

Proteolytic activity in liver cells from mouse, rat, Ehrlich ascites carcinoma bearing mouse and in Ehrlich ascites carcinoma cells.

The activity of intracellular proteinases from Ehrlich ascites carcinoma bearing mice were compared with that from liver cells of normal mice and rats. The activity of intracellular proteinases was measured in the supernatant of Ehrlich ascites carcinoma cells homogenate. The activity of intracellular proteinases in normal mouse and normal rat liver were different at pH 3.5, pH 6.0 and pH 7.5. The activity in liver cells from Ehlrich ascites carcinoma bearing mouse at pH 3.5 was not significantly changed from normal mouse or rat liver cells, however at pH 6.0 and pH 7.5 the activity in the affected liver significantly decreased. The proteolytic activity in the supernatant of Ehrlich ascites tumor cell homogenate was 0.110 E750 mmu/mgN at pH 7.5, 0.154 E750 mmu/mgN at pH 3.5. The proteolytic activity at pH 6.0 was not detected in any experiment.

Animals↗
PubMed1976

Macrophage migration inhibition-activity after implantation of methylcholanthrene-induced sarcoma, Ehrlich ascites cancer or mouse ascites hepatoma-134 cancer cells in mice.

Cells from methylcholanthrene-induced tumor (MC-tumor), Ehrlich ascites cancer or mouse ascites hepatoma (MH-134) were subcutaneously implanted in dorsal area of mice to examine the specific cell mediated immunity following implantation. The migration index (MI) of lymphocytes was determined at various time periods after cell transplantation. The MI-activity increased under all three implantations, reached maximum at a certain period, decreased gradually and disappeared. The maximum MI-activity coincided with the proliferation period of the implanted tumor cells. This peak occurred on the tenth postimplantation day with MC-tumors, on the fifth day with Ehrlich ascites cancer and on the sixth day with MH-134 cancer. In lymphoid tissues of animals with MC-tumor and Ehrlich ascites cancer, strong MI-activity appeared early in the regional axillary lymph nodes, while weak activity was observed consistently in the distant mesenterial lymph nodes. The MI-activity of the splenic lymphoid cells resembled the axillary lymph nodes cell activity. The MI-activity of venous blood lymphoid cells was parallel to the average value of lymphoid cells of the spleen and axillary and mesenterial lymph nodes.

Animals↗