pituitrin and Ascites

Hyponatremia is frequently seen in patients with ascites secondary to advanced cirrhosis and portal hypertension. Although not apparent in the early stages of cirrhosis, the progression of cirrhosis and portal hypertension leads to splanchnic vasodilation, and this leads to the activation of compensatory mechanisms such as renin-angiotensin-aldosterone system (RAAS), sympathetic nervous system, and antidiuretic hormone (ADH) to ameliorate low circulatory volume. The net effect is the avid retention of sodium and water to compensate for the low effective circulatory volume, resulting in the development of ascites. These compensatory mechanisms lead to impairment of the kidneys to eliminate solute-free water in decompensated cirrhosis. Nonosmotic secretion of antidiuretic hormone (ADH), also known as arginine vasopressin, further worsens excess water retention and thereby hyponatremia. The management of hyponatremia in this setting is a challenge as conventional therapies for hyponatremia including fluid restriction and correction of hypokalemia are frequently inefficacious. In this review, we discuss the pathophysiology, complications, and various treatment modalities, including albumin infusion, selective vasopressin receptor antagonists, or hypertonic saline for patients with severe hyponatremia and those awaiting liver transplantation.

Topics: Acute Kidney Injury; Acute-On-Chronic Liver Failure; Albumins; Antidiuretic Hormone Receptor Antagonists; Ascites; Fluid Therapy; Hepatic Encephalopathy; Hepatorenal Syndrome; Humans; Hypertension, Portal; Hyponatremia; Liver Cirrhosis; Liver Transplantation; Renin-Angiotensin System; Saline Solution, Hypertonic; Splanchnic Circulation; Tolvaptan; Vasodilation; Vasopressins

Topics: Antidiuretic Hormone Receptor Antagonists; Aquaporin 2; Ascites; Benzazepines; Diuretics; Humans; Japan; Liver Cirrhosis; Practice Guidelines as Topic; Receptors, Vasopressin; Signal Transduction; Sodium Potassium Chloride Symporter Inhibitors; Spironolactone; Tolvaptan; Vasopressins

Liver cirrhosis is a major cause of morbidity and mortality worldwide, mainly due to complications of portal hypertension. In this article, we review the current understanding on the pathophysiology, the diagnostic criteria and the available therapeutic options for patients with emerging hepatic syndromes in cirrhosis, namely the hepatorenal, hepato-adrenal and hepatopulmonary syndrome. The hepatorenal syndrome is a well-recognized complication of advanced cirrhosis and is usually associated with an accelerated course to death unless liver transplantation is performed. The hepatopulmonary syndrome is often missed in the evaluation of patients with cirrhosis; however, early recognition is essential for the efficient management of individual patients. The hepato-adrenal syndrome, although not fully characterized, offers an exciting field for research and potential therapeutic interventions.

Topics: Acute Kidney Injury; Adrenal Insufficiency; Ascites; Creatinine; Evidence-Based Medicine; Hepatorenal Syndrome; Humans; Hypertension, Portal; Liver Cirrhosis; Liver Transplantation; Lypressin; Midodrine; Norepinephrine; Octreotide; Plasma Substitutes; Portasystemic Shunt, Transjugular Intrahepatic; Serum Albumin; Terlipressin; Vasodilator Agents; Vasopressins

Hyponatremia is a frequent complication of advanced cirrhosis with ascites associated with increased morbidity and mortality. It is caused by an impairment in the renal capacity to eliminate solute-free water and is considered to be related to persistent secretion of vasopressin despite low serum osmolality. This nonosmotic release of vasopressin is mediated by the autonomic nervous system, which senses the underfilling of arterial vascular component. This reduction of effective arterial blood volume is closely related to the development of ascites. Although the short-time effects of vasopressin V2 receptor antagonists (vaptans) on hyponatremia and ascites have been repeatedly reported, their effects on the long-term management of cirrhotic ascites have not been established yet. Considering that their effects on water diuresis and their safety are limited by severe underfilling state of patients, cautious approaches with adequate monitoring are needed to advanced cirrhosis. Proper indication, adequate doses and new possibility of combination therapy should be explored in the future controlled study. As hyponatremia is frequent obstacle to ascites management, judicious combination with low-dose diuretics may decrease the incidence of refractory ascites. Although vaptans show much promise in the treatment of advanced cirrhosis, the problem of high cost should be solved for the future.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Aquaporin 2; Ascites; Biomarkers; Humans; Liver Cirrhosis; Neurophysins; Patient Selection; Protein Precursors; Receptors, Vasopressin; Risk Factors; Treatment Outcome; Vasopressins; Water-Electrolyte Balance

Hyponatremia is the most common electrolyte disorder in patients with cirrhosis. This disorder can be a result of substantial loss of extracellular fluid "hypotonic or hypovolemic hyponatremia" or develop in the context of an increase in extracellular fluid volume and in the absence of major sodium losses; this situation occurs in patients with advanced cirrhosis and is known as "dilutional or hypervolemic hyponatremia". In dilutional or hypervolemic hyponatremia, serum sodium concentration is reduced, plasma volume is increased (although the effective plasma volume is decreased due to marked arterial vasodilation in the splanchnic circulation) and extracellular fluid volume is increased, with ascites and edema in the absence of signs of dehydration. This is a result of the marked deterioration in renal excretion of solute-free water, leading to disproportionate water retention in relation to sodium retention. Hypotonic hyponatremia represents 10% of all hyponatremias in patients with cirrhosis. Since hypervolemic hyponatremia is by far the most frequent form of this disorder, the present chapter will concentrate specifically on hypervolemic hyponatremia in cirrhosis.

Topics: Antidiuretic Hormone Receptor Antagonists; Ascites; Blood Volume; Contraindications; Disease Progression; Diuresis; Extracellular Fluid; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney; Liver Cirrhosis; Liver Transplantation; Natriuresis; Prognosis; Saline Solution, Hypertonic; Splanchnic Circulation; Vasodilation; Vasopressins

Portal hypertension is one of the main consequences of cirrhosis. It results from a combination of increased intrahepatic vascular resistance and increased blood flow through the portal venous system. The condition leads to the formation of portosystemic collateral veins. Esophagogastric varices have the greatest clinical impact, with a risk of bleeding as high as 30% within 2 years of medium or large varices developing. Ascites, another important complication of advanced cirrhosis and severe portal hypertension, is sometimes refractory to treatment and is complicated by spontaneous bacterial peritonitis and hepatorenal syndrome. We describe the pathophysiology of portal hypertension and the current management of its complications, with emphasis on the prophylaxis and treatment of variceal bleeding and ascites.

Topics: Algorithms; Anti-Bacterial Agents; Ascites; Collateral Circulation; Diuretics; Endoscopy, Gastrointestinal; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Hepatorenal Syndrome; Hormones; Hypertension, Portal; Liver Cirrhosis; Lypressin; Peritonitis; Portasystemic Shunt, Transjugular Intrahepatic; Sclerotherapy; Secondary Prevention; Somatostatin; Spironolactone; Terlipressin; Vascular Resistance; Vasoconstrictor Agents; Vasodilation; Vasopressins

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Aquaporin 2; Aquaporin 6; Aquaporins; Ascites; Benzeneacetamides; Body Water; Demeclocycline; Diuresis; Diuretics; Humans; Kidney Tubules, Collecting; Liver Cirrhosis; Liver Cirrhosis, Experimental; Morpholines; Pyrrolidines; Rats; Receptors, Opioid, kappa; Receptors, Vasopressin; Spiro Compounds; Vasopressins

Topics: Adrenergic beta-Antagonists; Ascites; Carcinoma, Hepatocellular; Catheterization; Diuretics; Hemorrhage; Hepatic Encephalopathy; Humans; Hypertension, Portal; Liver Cirrhosis; Liver Neoplasms; Nitroglycerin; Peritonitis; Somatostatin; Vasopressins

Topics: Animals; Ascites; Body Water; Humans; Kidney; Liver Cirrhosis; Prostaglandins; Vasopressins

Topics: Ascites; Atrial Natriuretic Factor; Hemodynamics; Hepatorenal Syndrome; Humans; Liver Cirrhosis; Renin-Angiotensin System; Vasodilator Agents; Vasopressins

Hyponatremia complicates ascitic hepatic cirrhosis with frequency and gravity related to the gravity of the cirrhosis itself. When hyponatremia develops, it worsens the already present secondary hyperaldosteronism and makes therapy with spironolactone inefficacious. From a pathophysiologic viewpoint a pathogenetic role in determining hyponatremia is attributable to the reduced plasmatic renal perfusion; in several patients a syndrome of inappropriate ADH secretion develops. Other neurohormonal systems (catecholamines, prostaglandins, natriuretic hormones) are probably very important in modifying renal hemodynamics and renal tubular function. In some patients a causative role for hyponatremia is attributable to iatrogenic factors (e.g.: diuretics). From a therapeutic viewpoint, we examine some schedules, pharmacologic or not, that, however, are far from being useful for all patients. We discuss, mainly, water restriction, osmotic diuretics with or without loop diuretics, loop diuretics followed by sodium reintegration and concentration-reinfusion of ascites or application of peritoneovenous shunt.

Topics: Ascites; Humans; Hyponatremia; Liver Cirrhosis; Vasopressins

The ability of the kidneys to excrete sodium and free water is often impaired in patients with cirrhosis. Sodium retention is a sine qua non for ascites formation. The impairment of water excretion causes hyponatremia and hypo-osmolality. In addition, these patients frequently have functional renal failure caused by intense renal vasoconstriction. The renin-angiotensin-aldosterone system and the sympathetic nervous system, which are activated in most cirrhotic patients with ascites, and a nonosmotic hypersecretion of antidiuretic hormone are important mechanisms of sodium and water retention. Angiotensin II and sympathetic nervous activity may also be involved in the pathogenesis of functional renal failure. The renal production of prostaglandins is increased in cirrhotic patients with ascites as a homeostatic response to antagonize the vascular effect of endogenous vasoconstrictors and the tubular action of antidiuretic hormone. Nonsteroidal anti-inflammatory drugs should, therefore, be administered with caution in these patients because they may induce acute renal failure and water retention. Although sulindac inhibits the renal synthesis of prostaglandins in cirrhotic patients with ascites, it appears to have less effect on renal function than do other nonsteroidal anti-inflammatory drugs administered to these patients.

Topics: Anti-Inflammatory Agents; Ascites; Atrial Natriuretic Factor; Body Water; Diuretics; Hemodynamics; Humans; Kidney; Liver Cirrhosis; Prostaglandins; Renin-Angiotensin System; Sodium; Sulindac; Sympathetic Nervous System; Vasopressins

Topics: Age Factors; Animals; Ascites; Blood; Body Water; Heart Diseases; Humans; Kidney Failure, Chronic; Liver Cirrhosis; Osmolar Concentration; Rats; Renal Dialysis; Ultrafiltration; Vasopressins

Topics: Acidosis, Renal Tubular; Aldosterone; Ascites; Diuretics; Hepatic Encephalopathy; Humans; Hypokalemia; Kidney Failure, Chronic; Kidney Transplantation; Kidney Tubules, Distal; Liver Cirrhosis; Liver Transplantation; Sodium; Transplantation, Homologous; Uremia; Vasopressins; Water-Electrolyte Imbalance

Topics: Addison Disease; Ascites; Edema; Extracellular Space; Heart Failure; Humans; Hyponatremia; Intestinal Secretions; Kidney Failure, Chronic; Liver Cirrhosis; Potassium; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Aldosterone; Angiotensin II; Ascites; Humans; Juxtaglomerular Apparatus; Kidney; Liver; Liver Cirrhosis; Renin; Sodium; Vasopressins

Topics: Adrenal Cortex Hormones; Ascites; Bilirubin; Blood Pressure; Esophageal and Gastric Varices; Gastrectomy; Gastrointestinal Hemorrhage; Humans; Hypothermia, Induced; Osmosis; Plasmapheresis; Portacaval Shunt, Surgical; Portal Vein; Postoperative Care; Serum Albumin; Stomach; Tampons, Surgical; Vasopressins; Water-Electrolyte Balance

Topics: Adrenal Cortex Hormones; Aldosterone; Ascites; Diet Therapy; Edema; Humans; Liver Cirrhosis; Lymphatic System; Proteins; Vasopressins; Water-Electrolyte Balance

Water retention and dilutional hyponatremia, mainly attributable to an impairment of free water excretion and increased vasopressin activity, are well-documented complications in cirrhotic patients with ascites. VPA-985 is a selective, nonpeptide, orally active, vasopressin-2-receptor antagonist. The aim of this study was to determine the pharmacodynamics, safety, and pharmacokinetics of ascending single doses (25, 50, 100, 200, and 300 mg) in cirrhotic patients with ascites in a randomized, double-blind, placebo-controlled trial. Each dose level was studied in 5 patients (4 active and 1 placebo). After an overnight fast and fluid restriction (continued for 4 hours after dose administration), all patients were given placebo on baseline day and an oral suspension of VPA or placebo on the following day. VPA produced a significant dose-related increase in daily urine output (1,454 +/- 858 mL to 4,568 +/- 4,385 mL with VPA 300 mg) and a dose-related decrease in urine osmolality. The free water clearance reached greater than 3 mL/min for doses 100 mg or greater. Simultaneously, significant increases in serum osmolality, sodium, and vasopressin levels were found. There was a significant increase in sodium urine excretion. VPA was rapidly absorbed and maximum serum concentrations were achieved within 1 hour after administration. Elimination half-life ranged from 9.0 hours after 100 mg to 22.6 hours after 200 mg. In conclusion, VPA induced a dose-related aquaretic response, suggesting a therapeutic potential in managing water retention in patients with liver cirrhosis with ascites.

Topics: Adult; Aged; Antidiuretic Hormone Receptor Antagonists; Ascites; Azepines; Benzamides; Double-Blind Method; Drinking; Electrolytes; Female; Humans; Liver Cirrhosis; Male; Middle Aged; Osmolar Concentration; Pyrroles; Renin; Sodium; Urine; Urodynamics; Vasopressins; Water; Water-Electrolyte Balance

The activity of demeclotetracyclin, and ADH antagonist, is studied in 11 ethylic patients with cirrhosis of the liver, under a large hydric diet (1500 cm3). The prescription of the cyclin (600 mg daily) is always determined by a fall of the urinary osmolarity (-36%) and by a dramatic improvement of the free water clearance (+ 60%); consecutively, we observe an increase of natremia in 8 out of 9 cases. Associated with Spironolactone (200 mg daily) the anti-ADH activity persists (the free water clearance becomes positive in 5 out of 10 patients), in spite of the natriuretic activity of anti-aldosterone ; a minimal fall of the natremia is observed in only 2 cases. The indication of Demeclotetracyclin in the curative or preventive treatment of the hyponatremia of the liver cirrhosis is discussed.

Topics: Adult; Aged; Ascites; Clinical Trials as Topic; Demeclocycline; Drug Therapy, Combination; Edema; Female; Humans; Hyponatremia; Liver Cirrhosis; Male; Middle Aged; Natriuresis; Spironolactone; Vasopressins

The vasopressin system has emerged as a therapeutic focus for lowering portal hypertension and reducing splanchnic vasodilation in patients with refractory ascites. Clinically available vasopressin agonists are limited by preferential selectivity for V1 receptors that also have steep concentration-response curves with potential risks of excess vasoconstriction and/or complete antidiuretic effects. OCE-205 is a novel, selective, partial V1a receptor agonist with mixed agonist/antagonist activity and no V2 receptor activation at therapeutic doses. We carried out two studies assessing the in vivo effects of OCE-205 in different rat models of cirrhosis and ascites. In a carbon tetrachloride rat cirrhosis model, OCE-205 administration produced a marked reduction in portal hypertension and hyperaldosteronism, along with robust diuretic and natriuretic effects. These effects were accompanied by marked decreases in ascites volume, with three of five animals experiencing total mobilization of ascites. There was no evidence of fluid overload or sodium or water retention, confirming OCE-205's lack of V2 receptor activity. In a second, corroborative study using a bile duct ligation rat model of ascites, OCE-205 produced significant decreases in ascites volume and body weight and a significant increase in urine volume versus vehicle. Urine sodium excretion increased significantly after the first administration of OCE-205 relative to vehicle; however, repeat administration over 5 days did not lead to hyponatremia. Thus, in separate in vivo models, the mixed agonist/antagonist OCE-205 demonstrated relevant and expected endpoint findings consistent with its known mechanism of action and in vitro pharmacology without apparent unwanted effects or nonspecific toxicities.

Topics: Animals; Ascites; Diuretics; Hyperaldosteronism; Hypertension, Portal; Liver Cirrhosis; Natriuretic Agents; Rats; Receptors, Vasopressin; Sodium; Vasopressins

Catecholamines trigger proximal tubular fluid retention and reduce renal excretion of solute-free water. In advanced cirrhosis, non-osmotic hypersecretion of vasopressin (antidiuretic hormone or ADH) is considered the cause of dilutional hyponatraemia, but ADH V2 receptor antagonists are not beneficial in long-term treatment of ascites. To test the hypothesis that water retention in experimental ascitic cirrhosis might depend primarily on adrenergic hyper-function, hormonal status, renal function and tubular free-water reabsorption (TFWR) were assessed in six groups of rats with ascitic cirrhosis: rats with cirrhosis due to 13-week CCl4 (carbon tetrachloride) administration (group G1); cirrhotic rats receiving daily diuretics (0.5 mg/kg furosemide plus 2 mg/kg K(+)-canrenoate) from the 11th to the 13th week of CCl4 (G2), diuretics associated with guanfacine oral prodrug (α2A-adrenergic receptor agonist and sympatholytic agent) at 2 (G3), 7 (G4) or 10 (G5) mg/kg, or with SSP-004240F1 (V2 receptor antagonist) at 1 mg/kg (G6). Natriuresis was lower in G1 than in G2, G4 and G6 (all P<0.05). Guanfacine, added to diuretics (i.e. G3 compared with G2), reduced serum noradrenaline from 423±22 to 211±41 ng/l (P<0.05), plasma renin activity (PRA) from 35±8 to 9±2 ng/ml/h (P<0.05) and TFWR from 45±8 to 20±6 μl/min (P<0.01). TFWR correlated with plasma aldosterone (r=0.51, P<0.01) and urinary potassium excretion (r=0.90, P<0.001). In ascitic cirrhosis, reduced volaemia, use of diuretics (especially furosemide) and adrenergic hyper-function cause tubular retention of water. Suitable doses of sympatholytic agents are effective aquaretics.

Topics: Animals; Ascites; Canrenoic Acid; Diuretics; Furosemide; Guanfacine; Hyponatremia; Liver Cirrhosis, Experimental; Male; Natriuresis; Norepinephrine; Rats; Rats, Wistar; Vasopressins

To investigate the role of tolvaptan in regulating aquaporin (AQP)-2 expression and fecal water content in cirrhotic rats with ascites.. Cirrhosis with ascites was induced in rats by repetitive dorsal injection of CCl4 for 14 wk. In total, 84 cirrhotic rats with ascites divided into three groups (vehicle, 3 mg/kg and 5 mg/kg tolvaptan), and then further divided into five subgroups (days 1, 2, 3, 4, and 5). Blood samples were obtained to measure vasopressin and sodium concentrations. Rats were killed and colonic mucosa was scraped for analysis of protein expression and AQP-2 transcriptional level. The whole layer was fixed for hematoxylin&eosin (HE) staining and feces were collected for determination of fecal water content.. Compared with vehicle, vasopressin decreased significantly in the tolvaptan groups from day 2 to a similar level in each treatment group. AQP-2 showed significant upregulation in cirrhotic rats with ascites compared with an untreated control group (100% ± 22.9% vs 22.2% ± 10.23%, P < 0.01). After administration of tolvaptan, AQP-2 expression began to decrease significantly from day 2 in each treatment group, but no significant difference was finally found between the treatment groups. Fecal water content in the distal colon was increased by 5 mg/kg tolvaptan on day 1 (66.8% ± 9.3% vs 41.4% ± 6.3%, in the vehicle group, P < 0.05). Fecal water content returned to baseline at day 4 at the latest in both treatment groups, and did not correspond to the change in AQP-2 expression. HE staining of the colonic mucosa showed no mucosal damage related to tolvaptan.. Upregulation of AQP-2 in the distal colon is found in cirrhotic rats with ascites. Tolvaptan inhibits its expression and may decrease water reabsorption and induce diarrhea.

Topics: Animals; Aquaporin 2; Ascites; Benzazepines; Carbon Tetrachloride; Colon; Diarrhea; Dose-Response Relationship, Drug; Feces; Liver Cirrhosis, Experimental; Male; Rats, Sprague-Dawley; Sodium; Time Factors; Tolvaptan; Vasopressins; Water

The role of renal aquaporin-2 (AQP2) water channel turnover in patients with liver cirrhosis, portal hypertension and water retention remains unclear. Transjugular intrahepatic portosystemic shunt (TIPS) insertion reduces portal hypertension, improves water excretion and lowers plasma vasopressin. The aim of this study was to establish whether TIPS insertion decreases urinary AQP2 excretion (uAQP2) in parallel with improved water excretion.. Fourteen cirrhosis patients with refractory ascites were studied before TIPS insertion and 4 and 12 weeks after insertion. A 24-h urine collection was followed by an oral water load (20 ml/kg body weight) with a 4-h blood and urine sampling.. TIPS reduced the portal pressure gradient from a median 18(4) (25-75% InterQuartile-range) to 7(2) mmHg, p < 0.05 and the need for diuretics (p < 0.05). TIPS increased plasma sodium from 136(6) mmol/l to 139(4), (p < 0.05) and diuresis from 1650(1043) ml/24 h to 2230(560) (p < 0.05), although the 24-h urinary sodium excretion did not change. There was no change in the baseline uAQP2 before 274(249) ng/(mmol creatinine/24 h) and 12 weeks after TIPS 242(201). There were no systematic changes in uAQP2, plasma vasopressin or other vasoactive substances during the water loads, before or after TIPS.. The effective amelioration of portal hypertension improved the patient's water excretion and plasma sodium, but there was no change in renal AQP2 trafficking or vasopressin. These findings do not support a primary role for renal AQP2 water channels in portal hypertensive water retention.

Topics: Aquaporin 2; Ascites; Diuresis; Female; Humans; Hypertension, Portal; Liver Cirrhosis; Male; Middle Aged; Portal Pressure; Portasystemic Shunt, Transjugular Intrahepatic; Sodium; Vasopressins

Water retention in advanced cirrhosis and ascites may involve disturbances in renal distal tubular function and in the vasopressin system.. Twelve patients with Child B cirrhosis and ascites were compared with 11 patients with Child C cirrhosis and ascites. The subjects were studied during a 400 ml/h oral water load.. Child C patients had a lower baseline glomerular filtration rate (32 vs 63 ml/min, P<0.001) and a lower urinary flow rate (V(u)) (0.86 vs 1.95 ml/min, P<0.001) than the Child B patients. However, the free water clearance (C(H2O)) did not differ (-0.60 vs -0.21 ml/min, P=0.20). After the water loading, plasma vasopressin (AVP) decreased significantly in both the groups (P<0.05). The Child B patients had increased V(u) (1.95-3.24 ml/min, P<0.001) and C(H2O) (-0.21-1.21 ml/min, P<0.01) and distal fractional water excretion (10.5 vs 0% in Child C, P=0.01) and aquaporin-2 (AQP2) (P<0.058) after water loading. In contrast, the Child C patients did not have increased V(u) and C(H2O) in response to the water and the decrease in AVP. Furthermore, the markers of distal tubular water regulation, AQP2 excretion and distal fractional water excretion, were unaltered.. In Child C cirrhosis, ascites and mild hyponatraemia, there is an impaired ability to excrete solute-free water. The patients are characterised by a low glomerular filtration rate, a low distal tubular flow and an inability to increase free water clearance during water loading. This may be related to a vasopressin-independent production of AQP2.

Topics: Ascites; Body Water; Diuresis; Female; Humans; Kidney Tubules, Distal; Liver Cirrhosis; Male; Middle Aged; Severity of Illness Index; Vasopressins; Water-Electrolyte Imbalance

Nitric oxide has been proposed as a mediator of hyperdynamic circulation in cirrhosis. Endotoxin and cytokines induce the synthesis of nitric oxide. The aim of this study was to investigate the relationship between endotoxemia, cytokines, and nitric oxide in patients with cirrhosis, and to correlate these findings with clinical, biochemical, and hemodynamic parameters.. Clinical, biochemical, and hemodynamic parameters were assessed in 66 patients with cirrhosis and 15 controls. Levels of antidiuretic hormone, plasma renin activity, aldosterone, interferon gamma, interleukin-1, interleukin-6, tumor necrosis factor alpha, endotoxin, and nitrates-nitrites were determined.. Mean arterial pressure was lower and interleukin-6, tumor necrosis factor alpha, nitrites-nitrates levels, and endotoxin positivity rates were higher in cirrhotics than in controls (p < 0.005). Mean arterial pressure decreased and interleukin-6 levels increased with worsening of Child score (p < 0.005). Patients with ascites had higher levels of interleukin-6, tumor necrosis factor alpha, and nitrates-nitrites than patients without ascites (p < 0.01). Elevated levels of interleukin-6 were found in patients with encephalopathy grade I, compared with patients without (p < 0.001); this association was independent of the severity of liver disease. In patients with low mean arterial pressure, interleukin-6 levels were higher than in patients with high mean arterial pressure (p = 0.001), whereas tumor necrosis factor alpha and nitrates-nitrites levels were not different. By multivariate analysis, high interleukin-6 levels showed independent associations with the presence of ascites, encephalopathy, and low mean arterial pressure. Only interleukin-6 levels had significant correlations with Child score, plasma renin activity, serum and urinary sodium, and mean arterial pressure (r > or = 0.4, p < 0.005).. Although the activity of the nitric oxide pathway is increased in patients with cirrhosis and might contribute to the hemodynamic alteration, other factors are involved. Interleukin-6, possibly through nitric oxide-independent mechanisms, also might play a role in the vasodilatation of cirrhosis and the pathogenesis of hepatic encephalopathy.

Topics: Aged; Aldosterone; Ascites; Blood Pressure; Endotoxins; Female; Hepatic Encephalopathy; Humans; Interferon-gamma; Interleukin-1; Interleukin-6; Liver Cirrhosis; Male; Middle Aged; Nitrates; Nitric Oxide; Nitrites; Renin; Tumor Necrosis Factor-alpha; Vasopressins

The effects of the acute administration of arterial vasoconstrictors on renal plasma flow (RPF) and urinary sodium excretion (UNaV) in cirrhotic patients with ascites with or without hepatorenal syndrome (HRS) are still controversial. As a consequence, vasoconstrictors are not actually used in the treatment of renal sodium retention or HRS in these patients, regardless of the several lines of evidence suggesting that these renal functional abnormalities are related to a marked arterial vasodilation. The lack of an orally available effective arterial vasoconstrictor probably represents a further reason for this omission. Consequently, the present study was made to evaluate the acute effects of the oral administration of midodrine, an orally available -mimetic drug, on systemic and renal hemodynamics and on UNaV in cirrhotic patients with ascites. Mean arterial pressure (MAP), heart rate (HR), cardiac index (CI), systemic vascular resistance (SVR), left forearm blood flow (LFBF), left leg blood flow (LLBF), RPF, glomerular filtration rate (GFR), UNaV, plasma renin activity (PRA), plasma concentration of antidiuretic hormone (ADH), and the serum levels of nitrite and nitrate (NOx) were evaluated in 25 cirrhotic patients with ascites (17 without HRS and 8 with type 2 HRS) before and during the 6 hours following the oral administration of 15 mg of midodrine. During the first 3 hours after the drug administration, a significant increase in MAP (89.6 +/- 1.7 vs. 81.80 +/- 1.3 mm Hg; P < .0001) and SVR (1, 313.9 +/- 44.4 vs. 1,121.2 +/- 60.1 dyn . sec . cm-5; P < .0001) accompanied by a decrease in HR (69 +/- 2 vs. 77 +/- 3 bpm; P < .005) and CI (2,932.7 +/- 131.4 vs. 3,152.5 +/- 131.4 mL . min-1 . m2 BSA; P < .0025) was observed in patients without HRS. No change was observed in LFBF and LLBF. The improvement in systemic hemodynamics, which was also maintained during the the 3- to 6-hour period after midodrine administration, was accompanied by a significant increase in RPF (541.5 +/- 43.1 vs. 385.7 +/- 39.9 mL . min-1; P < .005), GFR (93.1 +/- 6.5 vs. 77.0 +/- 6.7 mL . min-1; P < .025), and UNaV (92.7 +/- 16.4 vs. 72.2 +/- 10.7 microEq . min-1; P < .025). In addition, a decrease in PRA (5.33 +/- 1.47 vs. 7.74 +/- 2.17 ng . mL-1 . h; P < .05), ADH (1.4 +/- 0.2 vs. 1.7 +/- 0.2 pg . mL-1; P < .05), and NOx (33.4 +/- 5.0 vs. 49.3 +/- 7.3 micromol-1; P < .05) was found. In patients with HRS, the effects of the drug on the systemic hemodynamics was smaller and shorte

Topics: Administration, Oral; Adrenergic alpha-Agonists; Ascites; Blood Pressure; Cardiac Output; Female; Glomerular Filtration Rate; Heart Rate; Hemodynamics; Humans; Kidney; Kidney Function Tests; Liver Cirrhosis; Male; Middle Aged; Midodrine; Nitrates; Nitrites; Regional Blood Flow; Renal Circulation; Renin; Vascular Resistance; Vasoconstriction; Vasopressins

To investigate a possible relationship between the renal production of endothelin and the presence of renal dysfunction and activation of vasoactive systems in cirrhosis, the urinary excretion and the circulating plasma levels of immunoreactive endothelin (irET) and the plasma levels of vasoactive hormones were measured in 19 healthy subjects, 12 cirrhotic patients without ascites and 39 patients with ascites and different degrees of renal dysfunction.. The urinary excretion and the circulating levels of irET were assessed after 5 days on a 40 mEq sodium diet and off diuretics. Renal function parameters and the plasma levels of vasoactive hormones were also measured.. Patients with and without ascites had similar values of urinary irET as compared with healthy subjects (30+/-3, 31+/-3 and 29+/-2 ng/day, respectively, p>0.10). By contrast, patients with ascites had higher circulating levels of irET (15+/-1.2 pg/ml) than patients without ascites and healthy subjects (11+/-1.6 and 5+/-0.4 pg/ml, p<0.01). In patients with cirrhosis, no correlation was found between urinary irET and circulating irET. Moreover, urinary irET did not correlate with liver tests, serum and urine sodium, glomerular filtration rate or vasoactive substances. Patients with hepatorenal syndrome had similar urinary irET to patients with ascites without hepatorenal syndrome.. Urinary excretion of irET is not increased in cirrhotic patients with ascites and does not correlate with abnormalities in renal function.

Topics: Adult; Aldosterone; Ascites; Atrial Natriuretic Factor; Endothelins; Female; Hepatorenal Syndrome; Humans; Liver Cirrhosis; Male; Middle Aged; Norepinephrine; Renin; Vasopressins

It has recently been described that kappa-opioid receptor agonists inhibit antidiuretic hormone secretion and promote water excretion in humans and experimental animals. The aim of this study was to evaluate the aquaretic efficacy of the kappa-opioid receptor agonist RU 51599 in conscious cirrhotic rats with ascites and water retention.. In protocol 1, arterial pressure, heart rate, and renal water metabolism were measured in basal conditions and then were measured for 120 minutes after the administration of Ringer's solution (n = 8; 0.4 mL) or RU 51599 (n = 7; 1 mg/kg). In protocol 2, plasma antidiuretic hormone concentration was measured (n = 6) before and 60 minutes after administration of RU 51599 (1 mg/kg). In protocol 3, the effect of RU 51599 (n = 9; 1 mg/kg) was compared with that of the V2-receptor antagonist SKF 100398 (n = 9; 30 micrograms/kg).. RU 51599 administration induced a profound diuretic and aquaretic effect without altering arterial pressure and heart rate. In protocol 2, the kappa-opioid agonist reduced by about 50% plasma antidiuretic hormone levels (from 6.6 +/- 0.9 to 3.4 +/- 0.6 pg/mL; P < 0.05). Finally, the improvement in renal water metabolism induced by RU 51599 was similar to that produced by the V2-receptor antagonist.. RU 51599 has a potent aquaretic effect in cirrhotic rats with water retention, suggesting that kappa-opioid receptor agonists may be useful for the treatment of water retention and dilutional hyponatremia in cirrhosis.

Topics: Analysis of Variance; Animals; Arginine Vasopressin; Ascites; Benzeneacetamides; Blood Pressure; Body Water; Diuresis; Heart Rate; Kidney; Liver Cirrhosis, Experimental; Male; Natriuresis; Pyrrolidines; Rats; Rats, Wistar; Receptors, Opioid, kappa; Vasopressins

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.

Topics: Angiotensin II; Animals; Arginine Vasopressin; Ascites; Blood Pressure; Hemodynamics; Homeostasis; Liver Cirrhosis, Experimental; Male; Rats; Rats, Inbred Strains; Receptors, Angiotensin; Receptors, Vasopressin; Vasopressins

Endogenous opioids may be involved in the pathogenesis of ascites and edema in patients with liver cirrhosis. We administered the opioid antagonist naloxone (5 mg bolus followed by a 0.06 mg/min infusion) to eight male patients with alcoholic cirrhosis and ascites and to five healthy age- and sex-matched control subjects and determined the effects of naloxone on water and electrolyte excretion after a nonsustained water load (20 ml/kg). In comparison with saline vehicle infusion carried out in the same subjects, naloxone administration resulted in a 50% increase in urine output and creatinine clearance and twofold increases in sodium and potassium excretion in patients with cirrhosis. Fractional sodium and potassium excretion, minimal urinary osmolality, plasma vasopressin and aldosterone levels, arterial blood pressure, and heart rate were not affected by naloxone treatment. The diuretic effect of naloxone was not observed in control subjects. Plasma naloxone levels were about six times higher in patients with cirrhosis than in control subjects (probably because of impaired metabolism of the drug) but only a weak correlation was found between drug levels and the degree of diuresis observed. The diuretic effect of naloxone may be related to an increase in glomerular filtration rate, possibly in conjunction with altered tubular reabsorption.

Topics: Aged; Aldosterone; Ascites; Blood Pressure; Body Water; Creatine; Electrolytes; Glomerular Filtration Rate; Heart Rate; Humans; Liver Cirrhosis; Male; Middle Aged; Naloxone; Potassium; Sodium; Vasopressins; Water-Electrolyte Balance

The pathogenetic role of ADH in determining hyponatremia in patients with liver cirrhosis is still much debated. Osmotic stimuli are not able to inhibit secretion of ADH in refractory ascites and under such conditions the reduction in effective plasma volume has been put forward as the main cause. Twenty patients with liver cirrhosis and refractory ascites were studied before and during extraction-concentration-reinfusion (ECR) of ascitic fluid by means of Rhodiascit. ADH, renin, aldosterone, blood and urine osmolarity, plasma and urinary concentration of sodium, potassium, chlorine, and the clearance of free water were evaluated. All patients presented high renin values (15.4 +/- 11.7 ng/ml), aldosterone (341 +/- 172 ng/ml), ADH (6.3 +/- 5.2 pg/ml). During ECR, a significant drop was observed in renin (p less than 0.001), aldosterone (p less than 0.001) urinary osmolarity (p less than 0.001) and an equality significant increase in diuresis (p less than 0.001), natriuria (p less than 0.005), kaliuria (p less than 0.001) while ADH presented an irregular course: in 11 cases it remained unchanged, in 3 it fell and in 6 it presented a constant increase. To conclude, data suggest that the diminished filtrate reaching the distal tubule constitutes the greatest cause of the inability to dilute urine in many patients with cirrhosis and that ADH is a permissive rather than a primary factor.

Topics: Aged; Aldosterone; Ascites; Female; Humans; Liver Cirrhosis; Male; Middle Aged; Potassium; Renin; Sodium; Vasopressins

Using multiple regression analysis, we have evaluated the clinical and hormonal conditions associated with impaired urinary sodium excretion in normoazotemic patients with cirrhosis and ascites. We retrospectively identified 13 patients with a urinary sodium excretion lower than 15 mmol/day and 13 patients with a sodium excretion higher than 15 mmol/day. Using univariate analysis, all the patients with poor sodium excretion had abnormally high levels of plasma renin activity, plasma aldosterone, and arginine vasopressin. In addition, they had a diastolic blood pressure lower than patients with high urinary sodium excretion, although otherwise were comparable as regards clinical and biochemical data. The consistency of the above associations was then tested by multiple-regression analysis in an attempt to control for potentially confounding factors and to identify only true, independent associations. After a discriminant stepwise procedure, we found that low diastolic blood pressure (P less than 0.01) and high plasma aldosterone levels (P less than 0.05) were the only two conditions independently associated with abnormally low urinary sodium excretion. These findings are consistent with the view that sodium retention in decompensated cirrhosis results from a concomitant severe contraction in the effective blood volume and an increased production and/or retention of aldosterone. The concordance between our results and several pathophysiological findings supports the validity of this statistical approach to confirm physiological and/or clinical predictions.

Topics: Adult; Aged; Aldosterone; Arginine; Ascites; Blood Pressure; Female; Humans; Liver Cirrhosis; Male; Middle Aged; Regression Analysis; Renin; Renin-Angiotensin System; Retrospective Studies; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Ascites; Body Water; Hepatorenal Syndrome; Humans; Hypertension, Portal; Kidney; Liver Circulation; Liver Cirrhosis; Lymph; Sodium; Vasopressins

To investigate the temporal relationship between the impairment of water excretion, sodium retention, and antidiuretic hormone hypersecretion in cirrhosis, free water excretion (estimated by the minimum urinary osmolality) and urinary antidiuretic hormone excretion (which correlates with the plasma levels of this hormone) were measured weekly after an oral water load in 18 rats with carbon tetrachloride-induced cirrhosis and in 20 control animals. The onset of ascites (as an index of sodium retention) in cirrhotic rats was estimated by sequential paracentesis. Thirteen cirrhotic animals developed an impairment of water excretion 2-5 wk after the onset of ascites. The urinary excretion of antidiuretic hormone in these animals, which was normal before the impairment of water excretion, increased markedly within the week in which this abnormality was first detected and remained high thereafter. The remaining 5 cirrhotic rats did not experience an impairment of free water excretion in spite of developing ascites. The urinary excretion of antidiuretic hormone in these animals was similar to that of control rats during the entire study. In all urine samples obtained from cirrhotic rats, there was a highly significant direct linear correlation between the urinary excretion of antidiuretic hormone and the minimum urinary osmolality. Our results show the following: in rats with carbon tetrachloride-induced cirrhosis, sodium retention preceded the impairment of water excretion; and in these animals, the defect in water metabolism correlated chronologically and quantitatively with antidiuretic hormone hypersecretion. These findings are consistent with the concept that antidiuretic hormone is a major determinant of the impaired water metabolism in cirrhosis.

Topics: Animals; Ascites; Body Water; Carbon Tetrachloride; Liver Cirrhosis, Experimental; Longitudinal Studies; Male; Osmolar Concentration; Rats; Rats, Inbred Strains; Vasopressins

In 5 patients with cirrhosis and ascites the glomerular filtration rate (GFR), free water clearance (CH2O) and urinary excretion of prostaglandin E2(PGE2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were measured before and after a 3-day treatment with sulindac (400 mg/day). The administration of sulindac induced a marked fall of urinary excretion of PGE2 (from 24.2 +/- 5.5 to 3.8 +/- 1.1 ng/h; p less than 0.05), 6-keto-PGF1 alpha (from 19.9 +/- 2.9 to 5.6 +/- 1.1 ng/h; p less than 0.02) GFR (from 111 +/- 15 to 67 +/- 10 ml/min; p less than 0.01) and CH2O (from 7 +/- 1.5 to 3.7 +/- 1.3 ml/min; p less than 0.02) in all patients studied. The plasma concentration of the active metabolite sulindac sulfide in cirrhotics was 400% of that found in 6 healthy volunteers (9.6 +/- 1.7 vs. 2.4 +/- 0.6 ng/ml). Our results indicate that sulindac, at a dose of 400 mg/day, inhibits the renal synthesis of prostaglandins and impairs renal function in cirrhotics with ascites. These effects are probably related to the marked alteration of sulindac kinetics that occurs in these patients.

Topics: 6-Ketoprostaglandin F1 alpha; Ascites; Body Water; Dinoprostone; Glomerular Filtration Rate; Humans; Indenes; Kidney; Kinetics; Liver Cirrhosis; Norepinephrine; Prostaglandins E; Renin; Sulindac; Vasopressins

A role for arginine vasopressin has been implicated in the compensatory control of arterial blood pressure in several animal models with reported increases in plasma levels of arginine vasopressin. A threefold elevation in plasma vasopressin has been reported in conscious dogs following constriction of the inferior vena cava. In the present study, infusion of the arginine vasopressin antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-O-methyltyrosine] Arg8-vasopressin into conscious dogs with chronic caval constriction did not decrease mean arterial blood pressure. However, the dose of infused antagonist completely blocked the pressor response to 2 micrograms of exogenous vasopressin. Also the antagonist produced no effect on heart rate, plasma renin activity, or urinary volume and electrolyte excretions. A slight, transient increase (P less than or equal to 0.05) was observed in creatinine clearance and in PAH clearance following antagonist infusion, suggesting a possible decrease in renal vascular resistance. These data suggest that the direct vasoconstrictor actions of vasopressin contribute minimally, if at all, to blood pressure maintenance following chronic caval constriction. Alternatively, blockade of endogenous vasopressin receptors at the level of peripheral arterioles may have resulted in no depressor response due to a masking of this response by other compensatory hormonal and neural pressor systems.

Topics: Animals; Arginine Vasopressin; Ascites; Dogs; Female; Hemodynamics; Receptors, Angiotensin; Receptors, Cell Surface; Receptors, Vasopressin; Renal Circulation; Renin; Sodium; Vasoconstriction; Vasopressins; Vena Cava, Inferior

Topics: Ascites; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Hypertension, Portal; Portal System; Propranolol; Sclerosing Solutions; Vasopressins

Topics: Ascites; Body Water; Humans; Hyponatremia; Kidney; Liver Cirrhosis; Peritoneovenous Shunt; Vasopressins

Following some remarks on the hyposomolar-hyponatraemic syndrome and on the formation of free water, the possible aetiopathogenetic mechanisms of hyponatraemia in ascitogenous cirrhosis of the liver and in particular the role of ADH are considered. 3 cases out of 18 suffering from ascitic phase cirrhosis in whom inability to produce free water was accompanied by conserved urinary excretion of sodium are reported. One explanation might be the intervention of ADH or of an antidiuretic substance.

Topics: Adult; Aged; Ascites; Female; Humans; Hyponatremia; Liver Cirrhosis; Male; Middle Aged; Osmolar Concentration; Vasopressins; Water-Electrolyte Imbalance

Sodium and water retention is constant in decompensated cirrhosis with ascites and edema. Sodium retention is due to several factors. Renal hemodynamic disturbances appear first: decrease in glomerular filtration and renal plasmatic perfusion, redistribution of renal perfusion to the juxtamedullar area where the longer nephrons reabsorb more sodium. Metabolic disorders of estrogens, natriuretic hormonal factor, prostaglandins and the kallikrein-kinin system contribute to greater sodium retention. Water retention is secondary to greater sodium reabsorption and to hyperactivity of the antidiuretic hormone. Sodium and water retention, associated with portal hypertension, with reduced oncotic pressure and with dynamic lymphatic insufficiency, is responsible for the production of ascites. The latter results in a decrease in the effective plasmatic volume, with non-suppression of the renin-angiotensin system, increased aldosterone production and additional sodium retention.

Topics: Ascites; Estrogens; Glomerular Filtration Rate; Humans; Kallikreins; Prostaglandins; Sodium; Vasopressins; Water-Electrolyte Imbalance

Topics: Ascites; Demeclocycline; Edema; Humans; Hyponatremia; Osmolar Concentration; Vasopressins; Water Intoxication

Plasma and urinary arginine vasopressin (AVP) in normal subjects and in patients with various water metabolism disorders was measured using a sensitive, specific radioimmunoassay. The AVP plasma levels in normal subjects were 3.1 +/- 1.2 pg/ml. The parallel changes in plasma osmolality, plasma AVP concentration, and urinary osmolality were observed after water load. In patients with various kinds of hyponatremia and impaired water excretion, plasma AVP concentrations were within or over normal levels, suggesting that persistent secretion of AVP may play an important role in the pathogenesis of hyponatremia. Variable levels of plasma AVP were observed in patients with essential hypernatremia, which in turn suggested that osmoreceptors may be selectively damaged in some patients, and that ADH-secreting neurons are also involved in others. Our radioimmunoassay facility made it possible for us to measure plasma and urinary DDAVP in the treatment of diabetes insipidus.

Topics: Adrenal Insufficiency; Adult; Animals; Arginine Vasopressin; Ascites; Diabetes Insipidus; Dogs; Edema; Humans; Hypernatremia; Hyponatremia; Hypotension, Orthostatic; Infant; Neoplasms; Osmolar Concentration; Radioimmunoassay; Vasopressins; Water

Topics: Adrenal Glands; Aldosterone; Ascites; Blood Pressure; Calcium; Creatinine; Cyclic AMP; Edema; Glomerular Filtration Rate; Humans; Hydrocortisone; Hypertension; Kidney; Kidney Failure, Chronic; Kidney Tubules; Liver Cirrhosis; Magnesium; Osmolar Concentration; Phosphates; Potassium; Prostaglandins; Renin; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Adrenal Insufficiency; Animals; Ascites; Diuresis; Edema; Heart Failure; Humans; Male; Methods; Rats; Vasopressins

Topics: Aldosterone; Aminohippuric Acids; Animals; Aorta; Ascites; Blood Pressure; Dogs; Edema; Female; Glomerular Filtration Rate; Heart Failure; Norepinephrine; Renin; Sodium; Tricuspid Valve; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Ascites; Diuretics; Ethacrynic Acid; Furosemide; Humans; Liver Cirrhosis; Magnesium; Male; Thiazines; Vasopressins

Topics: Adrenal Insufficiency; Ascites; Brain Injuries; Diabetes Insipidus; Eclampsia; Endocrine System Diseases; Female; Humans; Liver Cirrhosis; Oxytocin; Pregnancy; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Ascites; Humans; Liver Cirrhosis; Middle Aged; Vasopressins

Topics: Adolescent; Adult; Animals; Aortic Diseases; Ascites; Biological Assay; Blood; Dogs; Edema; Female; Heart Failure; Hematocrit; Humans; Male; Mitral Valve Insufficiency; Potassium; Secretory Rate; Sodium; Urine; Vasopressins; Venae Cavae

Topics: Ascites; Biomedical Research; Blood Gas Analysis; Blood Pressure; Bronchiectasis; Cardiovascular System; Heart; Oxytocin; Peptides; Pharmacology; Pulmonary Circulation; Pulmonary Emphysema; Pulmonary Fibrosis; Pulse; Respiration; Tuberculosis; Tuberculosis, Pulmonary; Vasopressins

Topics: Adrenocorticotropic Hormone; Aldosterone; Arginine Vasopressin; Ascites; Blood; Bradykinin; Cell Division; Cell Nucleus; Cortisone; Cricetinae; Estrone; Follicle Stimulating Hormone; Histamine; Hydrocortisone; In Vitro Techniques; Luteinizing Hormone; Microscopy; Microscopy, Phase-Contrast; Neoplasms; Neoplasms, Experimental; Oxytocin; Peptides; Pharmacology; Progesterone; Research; Serotonin; Testosterone; Tissue Culture Techniques; Vasopressins

Topics: Animals; Ascites; Carcinoma, Ehrlich Tumor; Chlorothiazide; Heparin; Histamine; Hydrocortisone; Mice; Neoplasms; Neoplasms, Experimental; Pharmacology; Radiation; Radiation Effects; Research; Vasopressins

Topics: Albumins; Arginine Vasopressin; Ascites; Blood Chemical Analysis; Humans; Liver Cirrhosis; Spiro Compounds; Urine; Vasopressins

Topics: Arginine Vasopressin; Ascites; Blood; Exudates and Transudates; Humans; Nephrosis; Vasopressins

Topics: Animals; Arginine Vasopressin; Ascites; Dogs; Electrolytes; Vasopressins

Topics: Ascites; Electrolytes; Humans; Liver Cirrhosis; Micrococcus; Vasopressins; Water