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PubMed1984

Management of ascites with hydrothorax.

Hydrothorax occurs in 5.3 percent of ascitic patients. Our experience with 22 cases forms the basis of this report. Of the 22 cases, 21 were spontaneous and 1 was due to transdiaphragmatic incision. Eighteen occurred on the right side. Usually fluid enters the chest through tiny defects in the diaphragm. These defects are often covered by pleuroperitoneum, but the high abdominal pressure raises a bleb on the superior surface of the diaphragm. Rupture produces hydrothorax. The ascites is often relieved with the onset of the hydrothorax. Blockage of the thoracic duct has produced chylous ascites. The thoracoabdominal communication is immediately confirmed by a scan of the chest and abdomen after intraperitoneal injection of technetium-99 colloid. Fluid is tapped from the chest immediately before intraperitoneal injection. The rate at which the technetium-99 enters the chest is related to the size of the defect in the diaphragm. A significant transfer should occur within 12 hours. Immediate transfer occurs with large defects. The ruptured blister on the diaphragm forms a one-way valve. Intrathoracic injection does not migrate into the peritoneal cavity. The valvular characteristics of the leak force ascitic fluid into the thorax because the differential pressure between the abdominal and pleural cavities is intensified by inspiration. If tension hydrothorax has occurred, urgent thoracocentesis and paracentesis may be required. A chest tube should not be introduced. The main principle of surgery is to supply a low resistance pathway for the return of fluid to the venous system and to eliminate the diaphragmatic defect by obliteration of the pleural space. A LeVeen peritoneovenous shunt is performed after emptying the abdomen of its fluid load. After completion of the shunt operation, the chest is emptied of fluid, and a sclerosing agent (tetracycline or nitrogen mustard) is injected into the pleural cavity. Closure of the defect is verified by technetium-99 labeled scans which also confirm shunt patency. With this regime, the defect closed or was rendered insignificant in 18 of 22 patients. One patient had a post-transdiaphragmatic surgical defect which was too extensive to be closed by the aforementioned procedures. One patient remained well but did not have closure of the defect, one patient with a ruptured hiatal hernia did not have closure, and one patient who had previous placement of a chest tube could not be closed. Therefore, 18 of 22 patients were successfully treated.

Ascites↗

PubMed1981

Isolation of alpha-actinin from sarcoma 180 ascites cells plasma membranes and comparison with smooth muscle alpha-actinin.

alpha-Actinin from Sarcoma 180 ascites cell plasma membranes was purified after extraction in 10 mM Tris, 1 mM EDTA, 1 mM mercaptoethanol, pH 8.5, by chromatography on DEAE and hydroxyapatite for comparisons with smooth muscles alpha-actinin purified from turkey gizzard by the same procedure. The two proteins were found to be very similar by sedimentation analysis, gel filtration and dodecyl sulfate gel electrophoresis. Direct comparisons of smooth muscle, skeletal muscle and ascites alpha-actinin by amino acid analysis indicated a closer relationship between the smooth muscle and ascites proteins than between the smooth and skeletal muscle proteins. Both smooth muscle and ascites alpha-actinins cross-link F-actin filaments. The results suggest that the smooth muscle protein is a better system for understanding properties of non-muscle alpha-actinins than is the skeletal muscle protein.

Actinin↗

PubMed1976

Apoprotein profile of plasma and chylous ascites lipoproteins.

Plasma and chylous ascites lipoproteins were compared in a rare case of exudative enteropathy associated with stenosis of the thoracic duct. All ascites lipoproteins separated by ultracentrifugation showed a much higher triglyceride/protein ratio and a lower cholesterol ester content than their plasma counterparts. Polyarcylamide gel electrophoresis of apoproteins before and after fractionation on Sephadex G-200 essentially showed, compared to normal plasma, a reduction of apoprotein C in VLDL and HDL particularly obvious for apoCIII1 and CIII2. Ascites lipoproteins were characterized by an increased apoA content in chylomicrons, VLDL and LDL and a reduced percentage of apo CII and CIII1, mostly in chylomicrons, VLDL and HDL. The differences in composition between plasma and ascites might be explained by different origins for the various apoprotein subfractions. The transsudation of chyle into the abdominal cavity might divert some peptides of intestinal origin from their normal entry into the circulation.

Apoproteins↗

PubMed1986

CA 125 (ovarian tumour-associated antigen) in ascitic liver diseases.

The presence of Ca 125, an ovarian cancer-associated antigen, was assessed in serum from patients with liver diseases with (n = 26) and without (n = 26) ascites. Abnormal levels of serum CA 125 were observed in all patients with ascites and in 4 patients without ascites (15%). We conclude that CA 125 is a non-specific marker of ascites whatever the origin: ovarian carcinoma, cirrhosis or peritoneal inflammatory process.

Antigens, Neoplasm↗

PubMed1989

Refractory ascites due to POEMS syndrome.

A 52-yr-old woman developed exudative ascites 2 yr after the onset of peripheral neuropathy. Extensive evaluation revealed that the patient had no underlying liver disease, malignancy, infection, or cardiac or renal disease. The ascites initially responded to high-dose corticosteroid therapy. The patient had many clinical features of the recently described POEMS syndrome, including a persistent IgA lambda-paraprotein. Initially, her ascites responded to treatment with steroids. This is characteristic of the syndrome and should be considered in patients with POEMS syndrome and refractory ascites.

Ascites↗

PubMed1990

Dextran-70 versus albumin as plasma expanders in cirrhotic patients with tense ascites treated with total paracentesis. Results of a randomized study.

To investigate whether albumin can be substituted by less expensive plasma expanders in cirrhotic patients with tense ascites treated with total paracentesis, 88 patients (16 with renal failure) submitted to this therapeutic procedure were randomly assigned to receive IV albumin (43 patients) or dextran-70. Both substances were given at a dose of 8 g/L of ascitic fluid removed. Patients were discharged from the hospital with diuretics, and cases developing tense ascites during follow-up were treated according to their initial schedule. Total paracentesis was effective in eliminating the ascites in all but two cases in each group. Neither paracentesis plus IV albumin infusion nor paracentesis plus IV dextran-70 infusion was associated with significant changes in renal and hepatic function or serum electrolytes. The incidence of renal impairment (one case in each group), hyponatremia (three and four cases, respectively), and other complications (hepatic encephalopathy, gastrointestinal hemorrhage, bacterial infections) after paracentesis, and the clinical course of the disease as estimated by the probability of readmission to hospital during follow-up, causes of readmission, probability of survival, and causes of death were similar in the two groups of patients. The effect of paracentesis on effective intravascular volume was indirectly assessed by measuring plasma renin activity and aldosterone concentration before and 2 and 6 days after treatment, the patients being without diuretics. In patients treated with albumin, no significant changes in renin and aldosterone were observed during the entire period of observation. In contrast, both parameters increased significantly on the 6th day of treatment in patients receiving dextran-70. A significant increase in plasma renin activity and aldosterone concentration (30% over baseline values) was observed in 51% of patients treated with dextran-70 and in only 15% of those treated with albumin (x2 = 10.4; P = 0.0012). These results indicate that although dextran-70 is less efficacious than albumin in protecting cirrhotic patients treated with total paracentesis from the decrease in effective intravascular volume, it appears to be capable of preventing the renal and electrolyte complications induced by this therapeutic procedure.

Adult↗

PubMed1991

Effect of V1-vasopressin receptor blockade on arterial pressure in conscious rats with cirrhosis and ascites.

Angiotensin II blockade with saralasin in human cirrhosis with ascites is associated with a significant reduction in arterial pressure, indicating that endogenous angiotensin II plays an important role in the maintenance of systemic hemodynamics in this condition. The aim of the current study was to investigate whether vasopressin also contributes to the maintenance of arterial pressure in cirrhosis with ascites. The study was performed using three groups of cirrhotic rats with ascites and three groups of control animals. The administration of d(CH2)5Tyr(Me)AVP, a selective antagonist of the vascular effect of vasopressin, to 10 cirrhotic rats induced a significant reduction in mean arterial pressure (from 94 +/- 4 to 85 +/- 4 mm Hg; P less than 0.001) and a significant increase in plasma renin activity (from 24.3 +/- 4.9 to 34.3 +/- 5.9 ng/mL.h; P less than 0.02) and plasma norepinephrine concentration (from 1474 +/- 133 to 2433 +/- 253 pg/mL; P less than 0.01). Similar results were observed following saralasin administration in a second group of 5 cirrhotic rats [mean arterial pressure decreased from 97 +/- 4 to 85 +/- 5 mm Hg (P less than 0.0001); and plasma renin activity and norepinephrine concentration increased from 18.4 +/- 5.8 to 40.3 +/- 5.7 ng/mL.h (P less than 0.02) and from 1383 +/- 70 to 2312 +/- 334 pg/mL (P less than 0.05), respectively]. The simultaneous blockade of angiotensin II and vasopressin in a third group of cirrhotic rats resulted in a significantly greater reduction of mean arterial pressure (from 97 +/- 6 to 74 +/- 6 mm Hg; P less than 0.05). No changes in arterial pressure were observed in the three groups of control rats. These findings indicate that endogenous vasopressin is as important as angiotensin II in the maintenance of arterial pressure in cirrhotic rats with ascites and support the contention that arterial hypotension is the initial event leading to the stimulation of the renin-angiotensin system and vasopressin in this animal model of cirrhosis.

Angiotensin II↗

PubMed1993

Peritoneovenous shunting restores atrial natriuretic factor responsiveness in refractory hepatic ascites.

BACKGROUND: Sodium retention in cirrhosis has been attributed to an imbalance between vasoconstrictive, antinatriuretic forces such as the renin aldosterone angiotensin system and the sympathetic nervous system, and vasodilatory, natriuretic agents such as atrial natriuretic factor (ANF). Patients with diuretic resistant refractory ascites may require peritoneovenous shunting (PVS) to control ascites. METHODS: To study the factors responsible for the improvement in sodium homeostasis post-PVS, we compared the response to ANF infusion before and 1 month after PVS in 6 patients with massive ascites. RESULTS: Before PVS, sodium excretion at baseline and in response to ANF infusion was blunted but became more normal post-PVS. ANF infusion post-PVS induced a significant increase in the glomerular filtration rate and filtration fraction and also in distal delivery of sodium. ANF's distal effect of increasing the fractional excretion of distally delivered sodium was present pre-PVS and was not significantly increased post-PVS. Changes in sodium handling were accompanied by a significant decrease in antinatriuretic forces (baseline aldosterone, 2079 +/- 507 vs. 647 +/- 17 nmol/L; P < 0.04) post-PVS. CONCLUSIONS: The improvement in sodium homeostasis and response to ANF infusion post-PVS appears to be associated with the decrease in antinatriuretic forces with the loss of massive refractory ascites. Thus, PVS restores the balance toward ANF responsiveness.

Adult↗

PubMed1993

Incidence, predictive factors, and prognosis of the hepatorenal syndrome in cirrhosis with ascites.

BACKGROUND: The aim of the study was to investigate the incidenc, predictive factors, and prognosis of the hepatorenal syndrome in cirrhosis with ascites. METHODS: The study is a follow-up investigation in 234 nonazotemic patients with cirrhosis and ascites. Thirty-nine variables obtained at inclusion were analyzed as possible predictors of hepatorenal syndrome occurrence (Kaplan-Meier method, Mantel-Cox test, and step-wise Cox regression procedure). RESULTS: The probability of hepatorenal syndrome occurrence was 18% at 1 year and 39% at 5 years. Sixteen variables had predictive value for hepatorenal syndrome occurrence in the univariate analysis: history of ascites, hepatomegaly, nutritional status, blood urea nitrogen level, serum creatinine concentration, serum sodium and potassium concentration, serum and urine osmolality, urinary sodium excretion, free water clearance after a water load, glomerular filtration rate, arterial pressure, plasma renin activity, plasma norepinephrine concentration, and esophageal varices. Neither etiology (alcoholic vs. nonalcoholic) nor the Child-Pugh score had predictive value. A multivariate analysis disclosed only three independent predictors of hepatorenal syndrome occurrence: low serum sodium concentration, high plasma renin activity, and absence of hepatomegaly. CONCLUSIONS: The hepatorenal syndrome is a relatively frequent complication in cirrhotic patients with ascites that is associated with an extremely short survival. Liver size, plasma renin activity, and serum sodium concentration are predictors of hepatorenal syndrome occurrence in these patients.

Adult↗

PubMed1977

Production of large amounts of antibodies, complement, and leukocytes in ascitic fluids of guinea pigs.

A method is described for the production in guinea pigs of large amounts of ascitic fluid containing non-specific IgG, antiprotein antibodies, complement, other serum proteins and leukocytes. The method is an adaptation of a procedure previously applied to mice. A major difference is the extended schedule of inoculations required for the induction of ascites in guinea pigs; a requirement for boosting with antigen intradermally while repeatedly inoculating adjuvant intraperitoneally; and the much larger quantities obtained. The average yield of ascitic fluid, when antigen was not used, was 113 ml per animal, and the average yield of IgG was 0.87 g. With antigen (keyhole limpet hemocyanin) the average yields were 143 ml and 1.6 g of antibody per guinea pig. Complement titers were 41 to 74% of those in serum. The number of leukocytes per ml of ascites ranged from 7 X 10(6) to 20 X 10(6). The method should be useful for the production of large amounts of leukocytes, antibodies and other serum proteins from a small colony of laboratory animals. In addition, cells can be obtained without the need to sacrifice the animal.

Animals↗

PubMed1985

One-step purification of mouse monoclonal antibodies from ascites fluid by hydroxylapatite chromatography.

A single-step method for purification of mouse monoclonal antibodies directly from ascitic fluids using hydroxylapatite column chromatography is described. The procedure yields highly purified IgG or IgM antibodies. The purified immunoglobulin is essentially free of contaminating mouse albumin, transferrin, and other ascites proteins, as determined by SDS-polyacrylamide gel electrophoresis. Hydroxylapatite chromatography can also separate monoclonal IgG antibodies from contaminating IgG antibodies found in ascites fluid of animals that have been immunosuppressed prior to ascites induction. Furthermore, the evidence presented here suggests that some hybridomas of SP2/0 origin synthesize an extraneous light chain resulting in the secretion of hybrid antibody molecules.

Animals↗

PubMed1990

Increased monoclonal antibody ascites production in mice primed with Freund's incomplete adjuvant.

The production of monoclonal antibodies is conveniently achieved by propagation of antibody-secreting hybridoma cells as ascites tumours in mice. With a view to improve production and minimise animal usage, the choice of primer (pristane or Freund's incomplete adjuvant (FIA] and the effect of sex of mouse (female vs. uncastrated male) upon antibody yields were compared. The volume of ascitic fluid harvested from 134 FIA-primed mice was 697 ml, which was significantly (P less than 0.02) greater than the 343 ml collected from 116 pristane-primed mice. Moreover, FIA-primed mice required tapping for only 11 days (90% in 7 days) compared to the 17 days needed for pristane-primed mice. While there was little difference between the mean IgG1 concentration (as determined by enzyme immunoassay) of both ascites pools (4.9 mg/ml compared to 4.6 mg/ml), the volume differences equated to yields of 25.5 mg/mouse and 13.5 mg/mouse respectively. The FIA-primed mice were also shown to produce on average more (P less than 0.02) ascites per day. There was no significant difference found between the yield of monoclonal antibodies obtained from either uncastrated males (22.1 mg/mouse) or females (23.1 mg/mouse). The use of FIA to prime mice for the in vivo production of monoclonal antibodies should improve the yield to over 20 mg/mouse, thereby reducing the number of mice required.

Animals↗

PubMed1993

Mice ascites as a source of polyclonal and monoclonal antibodies.

A large quantity of polyclonal anti-ovalbumin antibodies was obtained from mice by a simple modification of the method described by Kurpisz et al. (1988). In addition, the cells from ascitic fluid were used to produce monoclonal antibodies. Egg ovalbumin hyperimmunized BALB/c mice were injected successively with pristane, antigen and a non-antibody secreting myeloma cell line: the production of ascitic fluid containing antiovalbumin antibody activity was observed after 10-25 days. Cells from ascitic fluid were harvested, washed and fused together with polyethylene glycol to produce monoclonal antibodies. Two fusions were performed and a large number of monoclonal anti-ovalbumin antibodies was obtained. This method is simple, reproducible, allows many fusions to be obtained from one mouse, and allows the use of ascitic B cells rather than the more, frequently used splenic B cells.

Animals↗

PubMed1996

Evaluation of hollow fiber bioreactors as an alternative to murine ascites production for small scale monoclonal antibody production.

The objective of this study was to compare monoclonal antibody production in hollow fiber bioreactor systems and murine ascites to determine the feasibility of the bioreactor system as a potential alternative to the use of mice. Three hybridoma cell lines were grown in each of three different hollow fiber bioreactor systems and in groups of 20 mice. Mice were primed with 0.5 ml pristane intraperitoneally 14 days prior to inoculation of 1X10(6) hybridoma cells. Each mouse was tapped a maximum of three times for collection of ascites. Ascites volumes and daily clinical observations were recorded. Bioreactors were harvested three times weekly for 65 day and were monitored by cell counts, cell viability and media glucose consumption. Time and materials logs were maintained. The total quantity of monoclonal antibody produced in 20 mice versus the mean production for the three different bioreactors in 65 days was as follows: cell line 2B11, 455 mg vs. 168 mg; cell line 3C9, 446 mg vs. 565 mg; and cell line RMK, 997 mg vs. 1023 mg. Mean monoclonal antibody concentration ranged from 4.07 to 8.37 mg/ml in murine ascites, and from 0.71 to 11.10 mg/ml in hollow fiber bioreactor system. Although time and material costs were generally greater for the bioreactors, these results suggest that hollow fiber bioreactor system merit further investigations as potentially viable in vitro alternatives to the use of mice for small scale (< 1 g) monoclonal antibody production.

Animals↗

PubMed1983

Intraperitoneal xenon for the detection of early intestinal ischemia: effect of ascites, adhesions, and misdirected injections.

Significant delay in the washout of intraperitoneal xenon (133Xe) in rats and dogs with decreased splanchnic blood flow (bowel strangulation, superior mesenteric artery and vein occlusion) has been previously demonstrated as the basis for radionuclide imaging to detect early (prenecrotic) intestinal ischemia. In this study, the effect of ascites, adhesions, and misdirected injections on the validity of this technique is evaluated. Xenon-133 (0.6 mCi) in 3 ml saline was injected into the peritoneal cavity of anesthetized rats and the washout of gamma activity monitored externally for 90 min. Gamma camera images were obtained at 30-min intervals. After 60 min, only 12 +/- 2% of injected activity remained in the controls. Sham operation (13 +/- 1%) and simple obstruction (12 +/- 2%) had been previously shown not to significantly slow washout, but segmental strangulation had done so dramatically (32 +/- 2%, P less than 0.0001). In these experiments, ascitic fluid (Ringer's lactate) in volumes of 10 ml (13 +/- 1%), 20 ml (13 +/- 1%), and 40 ml (13 +/- 1%), did not significantly slow washout in nonischemic rats. Sixty and eighty milliliters produced very tense ascites and slight but significant delay in washout (14 +/- 1%, 17 +/- 1%, respectively, P less than 0.05). Moderate (11 +/- 1%) and severe (11 +/- 1%) adhesions produced by serosal scarification did not delay washout nor affect imaging. Injections of isotope intentionally misdirected into the abdominal wall (32 +/- 2%), bowel wall (18 +/- 1%), and bowel lumen (19 +/- 2%), each significantly (P less than 0.001) slowed washout. However, such misdirected injections were easily recognizable as such on the 1-min gamma camera images and could thereby be excluded as artifactual. Therefore, no false positive readings were obtained. It is concluded that the intraperitoneal xenon technique is not invalidated by mild to moderate ascites nor by moderate to severe adhesions. Misdirected injections produce invalid studies that are recognizable as such and thus are not misinterpreted. This approach should therefore be applicable to most patients with suspected intestinal ischemia.

Abdominal Muscles↗

PubMed1988

Presence of the atrial natriuretic factor (ANF) in human ascitic fluid.

Presence of atrial natriuretic factor (ANF)-like material was demonstrated by radioimmunoassay in ascitic fluid of 14 patients with cirrhosis of the liver. Immunoreactive ANF concentrations (M +/- SEM) were 2.4 +/- 0.5 fmol/ml in ascites, significantly lower (p less than 0.001) than the corresponding plasma concentrations of 15.5 +/- 2.6 fmol/ml. High performance gel permeation chromatography and reverse phase high performance chromatography of the ascitic ANF immunoreactivity showed correspondence to the alpha human ANF (99-126). ANF levels in ascites were significantly (p less than 0.01) correlated to levels in plasma (r = 0.66).

Ascites↗

PubMed1994

Mechanism of inhibitory actions of minocycline and doxycycline on ascitic fluid production induced by mouse fibrosarcoma cells.

Semisynthetic tetracyclines (TCNs) are used for the management of malignant pleural effusions as sclerosing agents. However, their precise mechanism of actions are uncertain. In the present study, the mechanism of inhibitory effects of minocycline (MINO) and doxycycline (DOXY), on the accumulation of ascitic fluid induced by mouse fibrosarcoma (Meth-A) cells were investigated using male mice. Meth-A cells inoculated intraperitoneally elicited 2.5-4 ml of bloody ascites 10 days after implantation. The production of ascitic fluid was suppressed in a dose-related manner by daily intraperitoneal injections of MINO or DOXY, whereas vehicle (normal saline with 0.01N HCl) did not exert a significant effect. The inhibitory activity of these two substances was quite similar; one mg/mouse of MINO or DOXY inhibited the accumulation of fluid by 87% and 84%, respectively. The survival rate of Meth-A-bearing mice treated with MINO or DOXY was higher than that of the controls. Macroscopic examination of the peritoneal cavity did not reveal any obvious effects, such as adhesions, in mice treated with either MINO or DOXY. In vitro studies showed that MINO and DOXY suppressed Meth-A cell growth with IC50s of 5 microM and 8 microM, respectively. Maximal suppression (95%) was achieved at MINO and DOXY concentrations of 25 microM. The above observations suggest that MINO and DOXY inhibit the accumulation of ascites by a direct effect on Meth-A cell growth. Therefore, it appears that TCNs injected into the pleural cavity to manage malignant effusions in man exert their activity, at least in part, by suppressing malignant cell growth.

Animals↗

PubMed1985

Rapid distribution of adriamycin in the ascitic and pleural fluid of women with ovarian carcinomas.

Adriamycin has been detected by high-pressure liquid chromatography in ascites and pleural fluid within 30 min after intravenous injection of Adriamycin (50 mg/m2). The concentration of Adriamycin was approximately one-half of that in plasma. Significant concentrations of Adriamycin metabolites were seen in the ascites fluid of one patient 4 hr after intravenous drug injection. Individual variability in the achievable ascites and pleural concentrations of cytotoxic drugs may be important in determining the responsiveness of patients to chemotherapy and the described analytical technique should be useful in assessing the concentrations of Adriamycin and its metabolites in malignant ascites and pleural effusions.

Ascitic Fluid↗