pituitrin and Liver-Diseases

This review will summarize the recent advances in our understanding of the relationship between liver and kidney function. It will outline the new concepts of the pathophysiology of renal dysfunction in chronic liver disease and examine novel renal biomarkers to detect acute kidney injury (AKI) in cirrhosis and following liver transplantation. We will further review new treatments for hepatorenal syndrome (HRS) and approaches to kidney dysfunction in liver transplantation recipients.. Recent studies evaluated the effect of the renin-angiotensin system on hepatic fibrosis and the role of the gut in mediating AKI after hepatic ischemia reperfusion injury. Multiple studies have investigated novel biomarkers such as neutrophil gelatinase-associated lipocalin to predict AKI (and HRS) in cirrhosis and after liver transplantation. Furthermore, there were recent advances in the management of kidney dysfunction including management of HRS with vasopressin analogs and kidney-sparing immunosuppression after liver transplantation.. Greater knowledge of the physiologic relationship between kidney and liver may open avenues for specific therapies of liver and kidney injury. Renal biomarkers may allow early diagnosis and targeted treatment of AKI, and improved management of kidney disease in the preliver and postliver transplantation setting will be crucial to improving long-term outcomes in these patients.

Topics: Acute Kidney Injury; Early Diagnosis; Female; Hepatorenal Syndrome; Humans; Immunosuppressive Agents; Liver Diseases; Liver Transplantation; Male; Renin-Angiotensin System; Vasopressins

Acute bleeding due to esophageal varices continues to be a life-threatening complication of liver disease. Despite the availability of improved therapy, mortality continues to be high. Octreotide has been shown to be at least as effective as vasopressin in the treatment of bleeding varices, with fewer and less severe systemic adverse effects. In addition, octreotide has also been consistently associated with a decreased need for transfusions. Octreotide has been used safely in patients without serious cardiovascular disease when administered as a continuous intravenous infusion of 25 micrograms/h for 24 hours with or without an initial 100-micrograms bolus dose. Since these trials have used small numbers of patients, the ability to detect small but clinically important differences has been limited. Additional controlled trials comparing octreotide with the combination of vasopressin and nitroglycerin are needed to more clearly determine the efficacy and cost-effectiveness of therapy. Furthermore, the optimal dosage, duration, and route of administration of octreotide in the treatment of bleeding esophageal varices has yet to be determined.

Topics: Clinical Trials as Topic; Esophageal and Gastric Varices; Gastrointestinal Agents; Gastrointestinal Hemorrhage; Hemostatics; Humans; Liver Diseases; Octreotide; Vasopressins

Topics: Adrenocorticotropic Hormone; Brain; Calcifediol; Calcium; Chronic Disease; Estradiol; Estrogens; Female; Follicle Stimulating Hormone; Glucose; Growth Hormone; Hormones; Humans; Hypothalamo-Hypophyseal System; Hypothyroidism; Insulin; Liver Cirrhosis, Alcoholic; Liver Diseases; Luteinizing Hormone; Male; Melatonin; Neurotransmitter Agents; Parathyroid Hormone; Phosphorus; Pituitary Gland; Prolactin; Renin-Angiotensin System; Somatomedins; Testosterone; Thyroid Hormones; Thyrotropin-Releasing Hormone; Vasopressins; Vitamin D

It is apparent that renal water retention in patients with advanced liver disease constitutes a fascinating clinical constellation with numerous and diverse causes and an elusive pathophysiology. The dissociation between elevated AVP levels and the attendant changes in renal water handling under diverse experimental conditions, and the demonstration of an impairment in renal water excretion in response to prostaglandin synthetase inhibition, underscore the multifactorial nature of the derangement. It is likely that the development of impaired renal water handling is attributable to a panoply of several hormonal or neural mediators, or both, acting in concert. Additional insight into this fascinating problem must await further characterization of some of the mediators and a delineation of their pathophysiologic role.

Topics: Body Water; Catecholamines; Glomerular Filtration Rate; Humans; Hyponatremia; Kidney; Liver Cirrhosis; Liver Diseases; Prostaglandins; Sympathetic Nervous System; Vasopressins; Water-Electrolyte Imbalance

Topics: Blood Coagulation; Blood Coagulation Disorders; Catecholamines; Contraceptives, Oral; Delivery, Obstetric; Factor VIII; Female; Humans; Immune System Diseases; Insulin; Kidney Diseases; Liver Diseases; Nicotinic Acids; Physical Exertion; Pregnancy; Pregnancy Complications; Surgical Procedures, Operative; Vasopressins

In patients with chronic liver disease a dissociation of the two most important partial functions of the adrenal cortex may be observed. A widening of the zona glomerulosa is associated with an increased aldosterone secretion and an atrophy of the zona fasciculata with a decreased cortisol production rate. In acute alcoholic liver damage there are sometimes remarkable special features concerning the adrenal function. The pathogenesis of the altered C21-steroid hormone metabolism is nonuniform and depends upon the etiology of the liver disease. Following factors may play role: 1. Decreased activity of specific hepatic enzymes a)direct enzyme damage b)indirect enzyme activity decreasing processed by deficiency of hydrogen from NADPH 2. Decreased hepatic blood flow 3. Disturbance of intracellular transport of substrates (e.g. cholestasis 4. Changes of transport proteins. 5. Direct or reactive changes of other factors of hormonal feedback systems (hypothalamus-pituitary-adrenal or gonadal-system; renin-angiotensin-aldosterone-system).

Topics: Adrenal Cortex; Adrenocorticotropic Hormone; Aldosterone; Chronic Disease; Circadian Rhythm; Cortisone; Glucocorticoids; Humans; Hydrocortisone; Liver Diseases; Male; Metyrapone; Mineralocorticoids; Steroids; Vasopressins

Topics: Budd-Chiari Syndrome; Chemical and Drug Induced Liver Injury; Collateral Circulation; Epinephrine; Hepatic Artery; Humans; Hypertension, Portal; Hypoxia; Liver Circulation; Liver Cirrhosis; Liver Diseases; Norepinephrine; Portal System; Vasopressins; Venous Pressure

Topics: Hemodynamics; Humans; Liver Circulation; Liver Diseases; Liver Function Tests; Splanchnic Nerves; Vasoconstrictor Agents; Vasopressins

Polycystic kidney disease (PKD) involves progressive hepatorenal cyst expansion and fibrosis, frequently leading to end-stage renal disease. Increased vasopressin and cAMP signaling, dysregulated calcium homeostasis, and hypertension play major roles in PKD progression. The guanylyl cyclase A agonist, B-type natriuretic peptide (BNP), stimulates cGMP and shows anti-fibrotic, anti-hypertensive, and vasopressin-suppressive effects, potentially counteracting PKD pathogenesis. Here, we assessed the impacts of guanylyl cyclase A activation on PKD progression in a rat model of PKD. Sustained BNP production significantly reduced kidney weight, renal cystic indexes and fibrosis, in concert with suppressed hepatic cystogenesis in vivo. In vitro, BNP decreased cystic epithelial cell proliferation, suppressed fibrotic gene expression, and increased intracellular calcium. Together, our data demonstrate multifaceted effects of sustained activation of guanylyl cyclase A on polycystic kidney and liver disease. Thus, targeting the guanylyl cyclase A-cGMP axis may provide a novel therapeutic strategy for hepatorenal fibrocystic diseases.

Topics: Animals; Cell Proliferation; Cyclic AMP; Cyclic GMP; Cysts; Disease Models, Animal; Disease Progression; Epithelial Cells; Female; Fibrosis; Genetic Vectors; Humans; Hypertension; Kidney; Liver; Liver Diseases; Male; Natriuretic Peptide, Brain; Parvovirinae; Polycystic Kidney, Autosomal Recessive; Rats; Rats, Sprague-Dawley; Receptors, Atrial Natriuretic Factor; Signal Transduction; Vasopressins

The neurohypophysial hormone arginine vasopressin (AVP) acts by three distinct receptor subtypes: V1a, V1b, and V2. In the liver, AVP is involved in ureogenesis, glycogenolysis, neoglucogenesis and regeneration. No data exist about the presence of AVP in the biliary epithelium. Cholangiocytes are the target cells in a number of animal models of cholestasis, including bile duct ligation (BDL), and in several human pathologies, such as polycystic liver disease characterized by the presence of cysts that bud from the biliary epithelium. In vivo, liver fragments from normal and BDL mice and rats as well as liver samples from normal and ADPKD patients were collected to evaluate: (i) intrahepatic bile duct mass by immunohistochemistry for cytokeratin-19; and (ii) expression of V1a, V1b and V2 by immunohistochemistry, immunofluorescence and real-time PCR. In vitro, small and large mouse cholangiocytes, H69 (non-malignant human cholangiocytes) and LCDE (human cholangiocytes from the cystic epithelium) were stimulated with vasopressin in the absence/presence of AVP antagonists such as OPC-31260 and Tolvaptan, before assessing cellular growth by MTT assay and cAMP levels. Cholangiocytes express V2 receptor that was upregulated following BDL and in ADPKD liver samples. Administration of AVP increased proliferation and cAMP levels of small cholangiocytes and LCDE cells. We found no effect in the proliferation of large mouse cholangiocytes and H69 cells. Increases were blocked by preincubation with the AVP antagonists. These results showed that AVP and its receptors may be important in the modulation of the proliferation rate of the biliary epithelium.

Topics: Animals; Bile Ducts, Intrahepatic; Cell Line; Cyclic AMP; Cysts; Epithelium; Humans; Keratin-19; Liver Diseases; Male; Mice, Inbred C57BL; Rats, Inbred F344; Receptors, Vasopressin; Vasopressins

We report measurements of the temporal response of serum vasopressin concentrations in the period after reperfusion of the liver graft during orthotopic liver transplantation (OLT).. Vasopressin concentrations were determined in 11 adult patients undergoing OLT by radioimmunoassay of samples collected after induction, at 5 minutes prior to reperfusion, and at 10, 20, 30, 40, 50, 60, 90, and 120 minutes after reperfusion.. Pre-incision vasopressin concentrations ranged from <0.5 to 2.6 pg/mL (reference serum vasopressin, <1.7 pg/mL). Overall, levels increased before reperfusion, but fell thereafter. Individual patients manifested elevated levels during the period after reperfusion. Values immediately before reperfusion exhibited most variability, ranging from 0.8 to 40 pg/mL (median, 15; interquartile range [IQR], 4-29) Median vasopressin concentrations 10 minutes postreperfusion were 7.6 pg/mL (IQR, 3-27). Only 3 of the 11 patients failed to generate vasopressin levels >20 pg/mL. In each of these patients, hemodynamics were satisfactory without the need for additional pressor infusion. Maximum vasopressin concentration measured in any patient was 85 pg/mL. There was no correlation between vasopressin concentration and mean blood pressure or systemic vascular resistance index.. Vasopressin concentrations during OLT vary widely and are elevated periodically during the anhepatic and postreperfusion stages, with no apparent relationship between vasopressin concentrations and blood pressure. Although vasopressin concentrations were not as high as those measured during some other clinical situations, these data suggest that a relative vasopressin deficiency is not a direct cause of hypotension during OLT.

Topics: Adult; Dopamine; Erythrocyte Transfusion; Humans; Liver Diseases; Liver Transplantation; Monitoring, Intraoperative; Reperfusion; Transplantation, Homologous; Vasopressins

Portal hypertension is associated with splanchnic vasodilation which is claimed responsible for the maintenance of chronically elevated portal pressure. Vasopressin analogues are used in the treatment of acute variceal bleeding, since they effectively reduce splanchnic blood flow and portal pressure. Dehydration stimulates the release of endogenous vasopressin release. Here we compared the effects of deprivation of drinking water for 18 h with those of vasopressin infusion on mesenteric hemodynamics in portal vein-ligated (PVL) and sham-operated (SHAM) rats. Blood flow in the superior mesenteric artery was measured with the ultrasonic transit time shift technique. Deprivation of drinking water had no hemodynamic effects in SHAM rats, but completely reversed the mesenteric hyperemia and portal hypertension in PVL rats to figures measured in SHAM rats, without altering blood pressure. Similarly, intravenous infusion of low doses of arginine vasopressin (1-10 pmol/min) selectively reduced mesenteric blood flow in PVL rats but had little effect in SHAM rats. These data suggest that control of water balance or aquaretic drugs might have beneficial effects on splanchnic hemodynamics and portal pressure in advanced liver disease, possibly by stimulating endogenous vasopressin release.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Disease Models, Animal; Hyperemia; Hypertension, Portal; Ligation; Liver Diseases; Male; Mesenteric Artery, Superior; Portal Vein; Rats; Rats, Sprague-Dawley; Splanchnic Circulation; Vasoconstrictor Agents; Vasodilation; Vasopressins; Water Deprivation

Topics: Abdomen, Acute; Adult; Aged; Hemostatics; Humans; Liver Diseases; Male; Middle Aged; Multiple Trauma; Pancreatic Neoplasms; Pancreaticoduodenectomy; Rupture, Spontaneous; Vasopressins; Water-Electrolyte Imbalance

In a porcine model of uncontrolled hemorrhagic shock, we evaluated the effects of vasopressin versus an equal volume of saline placebo versus fluid resuscitation on hemodynamic variables and short-term survival. Twenty-one anesthetized pigs were subjected to severe liver injury. When mean arterial blood pressure was <20 mm Hg and heart rate decreased, pigs randomly received either vasopressin IV (0.4 U/kg; n = 7), an equal volume of saline placebo (n = 7), or fluid resuscitation (1000 mL each of lactated Ringer's solution and hetastarch; n = 7). Thirty minutes after intervention, surviving pigs were fluid resuscitated while bleeding was surgically controlled. Mean (+/- SEM) arterial blood pressure 5 min after the intervention was significantly (P < 0.05) higher after vasopressin than with saline placebo or fluid resuscitation (58 +/- 9 versus 7 +/- 3 versus 32 +/- 6 mm Hg, respectively). Vasopressin improved abdominal organ blood flow but did not cause further blood loss (vasopressin versus saline placebo versus fluid resuscitation 10 min after intervention, 1343 +/- 60 versus 1350 +/- 22 versus 2536 +/- 93 mL, respectively; P < 0.01). Seven of 7 vasopressin pigs survived until bleeding was controlled and 60 min thereafter, whereas 7 of 7 saline placebo and 7 of 7 fluid resuscitation pigs died (P < 0.01). We conclude that vasopressin, but not saline placebo or fluid resuscitation, significantly improves short-term survival during uncontrolled hemorrhagic shock.. Although IV fluid administration is the mainstay of nonsurgical management of trauma patients with uncontrolled hemorrhagic shock, the efficacy of this strategy has been discussed controversially. In this animal model of severe liver trauma with uncontrolled hemorrhagic shock, vasopressin, but not saline placebo or fluid resuscitation, improved short-term survival.

Topics: Animals; Blood Flow Velocity; Blood Pressure; Female; Fluid Therapy; Heart Rate; Liver Diseases; Male; Resuscitation; Shock, Hemorrhagic; Survival Rate; Swine; Treatment Outcome; Vasopressins

Vasopressin has been reported to reduce bile flow, but its effects on bile acid secretion and bile acid-related hepatotoxicity are still unclear. We therefore investigated the influence of vasopressin on the hepatotoxicity and biliary excretion of taurochenodeoxycholic acid in primary cultured rat hepatocytes and isolated perfused rat liver models.. 1) Addition of vasopressin to hepatocyte cultures significantly decreased lactate dehydrogenase release as compared to cultures exposed to 1 mM taurochenodeoxycholic acid alone, and also reduced intracellular taurochenodeoxycholic acid content from 19.3 +/- 2.2 to 13.0 +/- 1.6 nmol/mg protein. After 30 min of preincubation with 1 mM taurochenodeoxycholic acid, rinsing and reculture of hepatocytes in bile acid-free medium resulted in gradual decrease in the intracellular level of the bile acid, and addition of vasopressin (10(-9) M) to the reculture medium accelerated this process. 2) Superimposition of vasopressin (330 pmol/l) for 10 min on taurochenodeoxycholic acid infusion (1.0 mumol/min: 25 mumol/l) caused a rapid increase in bile flow and biliary excretion of taurochenodeoxycholic acid (697 +/- 42 vs 584 +/- 27 nmol/10 min per g liver) from perfused rat livers, and significantly reduced lactate dehydrogenase release. 3) Superimposition of the PKC blocker H-7 (5 mumol/l) on taurochenodeoxycholic acid infusion (1.0 mumol/min: 25 mumol/l) caused a gradual increase in bile flow and biliary excretion of taurochenodeoxycholic acid. Furthermore, an additional infusion of vasopressin (100 pmol/l) for 10 min in the presence of H-7 produced a greater increase in bile flow and biliary excretion of taurochenodeoxycholic acid as compared with H-7 alone (754 +/- 71 vs. 657 +/- 26 nmol/g liver). 4) Continuous infusion of vasopressin (330 pmol/l) significantly increased the late peak (10-50 min) of horseradish peroxidase excretion from perfused livers (from 8.48 +/- 1.02 to 21.7 +/- 6.02 ng/g liver).. These findings suggest that vasopressin exerts a protective effect against taurochenodeoxycholic acid-induced hepatotoxicity by stimulating the secretion of this bile acid via intracellular vesicular transport systems.

Topics: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; Bile; Cells, Cultured; Cholagogues and Choleretics; Enzyme Inhibitors; Horseradish Peroxidase; L-Lactate Dehydrogenase; Liver; Liver Diseases; Male; Perfusion; Rats; Rats, Sprague-Dawley; Secretory Rate; Taurochenodeoxycholic Acid; Vasopressins

The influence of vasopressin and epinephrine on hepatic energy metabolism in the state of brain death was assessed by measuring arterial ketone body ratio (AKBR) and hepatic energy charge (EC) in brain-dead dogs. Mean arterial blood pressure (MABP) was significantly decreased from 125.5 +/- 5.5 to 53.4 +/- 1.7 mmHg after complete brain death (P less than 0.01). In the control group AKBR and EC were maintained at near the normal values thereafter, despite marked hypotension. Combined administration of vasopressin and epinephrine sustained AKBR normally and improved MABP above 90 mmHg (P less than 0.01). EC was also maintained within the normal range at 5 hr after initiation of administration of the drugs. By contrast, vasopressin or epinephrine alone maintained AKBR and EC at near the normal values, but improved MABP just slightly to around 60 mmHg (P less than 0.01). As for the volume control, the urinary output was significantly smaller in the vasopressin and epinephrine-treated group than in the control group (P less than 0.05). It is suggested that combined administration of vasopressin and epinephrine has a synergistic effect in improving the hemodynamics and maintenance of the energy status of the liver. This regimen is recommended as a good one for maintaining potential liver donors in the state of brain death.

Topics: Adenine Nucleotides; Animals; Arteries; Blood Pressure; Brain Death; Dogs; Drug Synergism; Energy Metabolism; Epinephrine; Female; Graft Survival; Ketone Bodies; Liver; Liver Diseases; Liver Transplantation; Male; Tissue Donors; Vasopressins

We evaluated the changes in the hepatic hemodynamics and blood ketone body ratio (KBR) induced by vasopressin in 40 patients with chronic liver diseases to clarify the effect of hepatic blood flow on hepatic energy charge expressed by KBR. Following infusion of vasopressin, the rate of decrease in portal blood flow in liver cirrhosis (LC) was significantly lower than that in chronic hepatitis (CH). Moreover, the blood flow in the hepatic artery after vasopressin infusion was greater in LC than in CH. As a result, the total hepatic blood flow, which was the sum of the flow in the above two vessels, after vasopressin infusion was greater in LC than in CH but the decrease in the blood KBR was not significant in LC. Thus, vasopressin appears to be hemodynamically safe in patients with LC, but caution is needed since it may decrease blood pressure, total hepatic blood flow and KBR in some LC patients.

Topics: Adult; Chronic Disease; Energy Metabolism; Hemodynamics; Humans; Infusions, Intravenous; Ketone Bodies; Liver; Liver Circulation; Liver Diseases; Middle Aged; Vasopressins

Topics: Cyclosporins; Humans; Liver Diseases; Liver Transplantation; Methylprednisolone; Prednisone; Urine; Vasopressins

One of the may vital functions of the liver is the biodegradation of foreign substances. The enzyme systems responsible for this liver function are frequently the site of drug interactions, both therapeutic and detrimental. Various substances can alter these enzymes by inducing, inhibiting, or competing with them, thus affecting drug response. In most instances, the liver detoxifies and deactivates chemicals, protecting the body from their harmful effects. In some biotransformation processes, however, toxic metabolites are produced that may be injurious to liver tissue as well as other body organs and systems. The effect of alcohol on the liver is a prime example. Although significant strides have been made in recent years, much is yet to be learned concerning the effect of the liver on drugs, the effect of drugs on the liver, and the pharmacologic management of various liver diseases.

Topics: Acetaldehyde; Alcoholism; Chemical and Drug Induced Liver Injury; Diuretics; Drug-Related Side Effects and Adverse Reactions; Ethanol; Hepatic Encephalopathy; Humans; Inactivation, Metabolic; Lactulose; Levodopa; Liver; Liver Cirrhosis; Liver Diseases; Microsomes, Liver; Neomycin; Oxidation-Reduction; Pharmaceutical Preparations; Spironolactone; Vasopressins

Topics: Acid-Base Imbalance; Adult; Alcoholism; Beer; Heart Diseases; Humans; Hyponatremia; Liver Diseases; Male; Nutrition Disorders; Vasopressins

Seventeen patients bleeding from oesophageal varices were treated by continuous infusion of vasopressin through a catheter inserted percutaneously and positioned in the superior mesenteric artery and in two other patients catheterization proved technically impossible. Bleeding was completely controlled on only four out of 18 occasions in the 17 patients treated. In seven patients, bleeding was controlled for two or more days but then recurred although the infusion was continued with an increased dose of vasopressin. There was a high incidence of complications, including bleeding from the site of catheter insertion in the groin and septicaemias. Sengstaken balloon tamponade and oesophageal transection had to be used to control bleeding in some patients but only six out of 17 survived to leave hospital.

Topics: Adult; Catheterization; Endocarditis, Bacterial; Esophageal and Gastric Varices; Female; Gastrointestinal Hemorrhage; Heart Arrest; Humans; Injections, Intra-Arterial; Liver Diseases; Male; Meningitis, Pneumococcal; Mesenteric Arteries; Middle Aged; Radiography; Thromboembolism; Vasopressins

Topics: Aminocaproates; Blood Coagulation Disorders; Blood Transfusion; Duodenal Ulcer; Esophageal and Gastric Varices; Esophagitis; Fibrinogen; Fibrinolysis; Gastritis; Gastrointestinal Hemorrhage; Heparin; Humans; Liver Diseases; Phosphorus Isotopes; Portacaval Shunt, Surgical; Stomach Ulcer; Therapeutic Irrigation; Vasopressins; Vitamin K

Topics: Acid-Base Equilibrium; Adult; Aged; Blood Pressure Determination; Catheterization; Electrocardiography; Esophageal Neoplasms; Female; Hematocrit; Hodgkin Disease; Humans; Hypertension, Portal; Liver Cirrhosis; Liver Diseases; Lysine; Male; Methods; Middle Aged; Phenylalanine; Portal System; Respiratory Function Tests; Umbilical Veins; Valsalva Maneuver; Vasopressins; Venous Pressure

Topics: Blood Circulation; Heart; Hemodynamics; Humans; Liver Diseases; Vasopressins

Topics: Ammonium Chloride; Animals; Bicarbonates; Blood Flow Velocity; Blood Gas Analysis; Carbon Dioxide; Cyanides; Dogs; Glucagon; Heart Arrest; Heart Failure; Humans; Hydrogen-Ion Concentration; Liver Diseases; Lymph; Oxygen; Oxygen Consumption; Shock, Hemorrhagic; Thoracic Duct; Vasopressins

Topics: Adrenocorticotropic Hormone; Cushing Syndrome; Female; Humans; Hydrocortisone; Insulin; Liver Diseases; Metyrapone; Myxedema; Obesity; Pituitary-Adrenal Function Tests; Pregnancy; Vasopressins

Topics: Amphetamine; Amyl Nitrite; Atropine; Edema; Female; Humans; Liver Diseases; Myxedema; Pre-Eclampsia; Pregnancy; Premenstrual Syndrome; Sodium Chloride; Vasopressins

Topics: Animals; Diuresis; Dogs; Liver Diseases; Vasopressins; Water-Electrolyte Balance

Topics: Diuretics; Edema; Heart Failure; Kidney Diseases; Liver Diseases; Organomercury Compounds; Physiology; Vasopressins

Topics: Blood Transfusion; Cryosurgery; Esophageal and Gastric Varices; Gastric Hypothermia; Hematemesis; Hypertension; Hypertension, Portal; Hypothermia, Induced; Liver Cirrhosis; Liver Diseases; Neomycin; Prognosis; Surgical Procedures, Operative; Vasopressins

Topics: Adrenocorticotropic Hormone; Cushing Syndrome; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diabetic Nephropathies; Endocrine Glands; Endocrine System Diseases; Hormones; Humans; Hypercalcemia; Hypothyroidism; Liver Diseases; Lung Neoplasms; Neoplasms; Nephrosis; Polycythemia; Pseudopseudohypoparathyroidism; Vasopressins

Topics: Adrenal Cortex Hormones; Diuretics; Gonadal Steroid Hormones; Humans; Liver Diseases; Vasopressins

Topics: Arginine Vasopressin; Diuretics; Liver Diseases; Vasopressins

Topics: Diabetes Insipidus; Humans; Liver Diseases; Vasopressins

Topics: Aldosterone; Arginine Vasopressin; Body Fluids; Deamino Arginine Vasopressin; Humans; Liver Diseases; Vasopressins

Topics: Arginine Vasopressin; Body Fluids; Liver Diseases; Vasopressins; Water-Electrolyte Balance

Topics: Arginine Vasopressin; Humans; Liver Diseases; Urinary Tract Physiological Phenomena; Vasopressins

Topics: Arginine Vasopressin; Body Fluids; Humans; Liver Diseases; Sodium Chloride; Vasopressins; Water

Topics: Arginine Vasopressin; Edema; Liver Diseases; Vasopressins

Topics: Animals; Arginine Vasopressin; Diet, Protein-Restricted; Liver Diseases; Protein Deficiency; Rats; Urine; Vasopressins

Topics: Humans; Liver Cirrhosis; Liver Diseases; Vasopressins; Water

Topics: Diuresis; Humans; Liver Cirrhosis; Liver Diseases; Nicotine; Vasopressins

Topics: Arginine Vasopressin; Deamino Arginine Vasopressin; Liver Diseases; Minerals; Vasopressins; Water

Topics: Animals; Diuresis; Diuretics; Hormones; Liver Diseases; Pituitary Gland; Pituitary Gland, Posterior; Rats; Vasopressins

Topics: Edema; Electrolytes; Liver Diseases; Renal Elimination; Vasopressins; Water