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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:[The physiopathology of ascites]. 46 62

1. The mineralocorticoid 9 alpha-fluorohydrocortisone was given to 12 patients with cirrhosis without ascites. In seven an 'escape' from its sodium-retaining effects was observed, the other five continuing to retain sodium. 2. Changes in plasma renin activity (PRA) and inulin clearance (Cinulin) were used in the assessment of possible changes in the 'effective' extracellular fluid volume. PRA fell and Cinulin increased to a similar extent in each of the two groups of patients. The findings do not support the concept that the failure to show the mineralocorticoid escape in some patients with cirrhosis is due to a failure of expansion of the effective extracellular fluid volume. 3. Sodium reabsorption in the different segments of the nephron as estimated by clearance techniques under conditions of maximal water diuresis showed that the greatest changes to account for both mineralocorticoid escape and sodium retention were in the part of the nephron beyond the diluting segment.
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PMID:Studies on mineralocorticoid 'escape' in cirrhosis. 47 24

In the present study, we undertook to examine the relationship between urinary sodium retention and systemic hemodynamics in dogs with experimental portal cirrhosis induced by the sporadic feeding of dimethylnitrosamine. Sodium handling was studied by blanace techniques; plasma volume was measured serially with Evan's blue; and CO, blood pressure, CVP, and PVR were monitored through indwelling catheters. Six dogs were studied while standing quietly in a Pavlov sling, in a serial fashion starting 4 weeks after drug administration and continuing for some 3 months thereafter, until all dogs developed cirrhosis and ascites. Urinary sodium retention commenced generally between the ninth to twelfth week following the initation of treatment, but renal perfusion remained normal. Plasma volume expansion was noted within 1 week following the onset of sodium retention. Ascites was generally detected about 2 weeks following the initiation of sodium retention. No alteration in CO or PVR could be detected until ascites was present in significant amount. At that time, CO rose and PVR fell by about 20%. ABP tended to fall during the period of observation, but this was not significant. The initiation of sodium retention in this canine model does not depend on antecedent changes in CO or PVR.
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PMID:Temporal relationships between urinary salt retention and altered systemic hemodynamics in dogs with experimental cirrhosis. 71 96

We studied the effects of fenoldopam, a selective dopamine DA1 agonist on systemic and splanchnic hemodynamics, renal blood flow and sodium excretion in 12 patients with alcoholic cirrhosis and ascites. Hepatic, azygos and renal veins were catheterized before and after intravenous administration of fenoldopam, 0.05 micrograms/kg/min for 1 hr and increased to 0.1 micrograms/kg/min for another hour. Mean arterial pressure progressively decreased (from 83 +/- 7 to a minimum of 77 +/- 8 mm Hg 100 min after starting the infusion) but returned to baseline level at 120 min. Plasma norepinephrine and renin activity increased (respectively from 567 +/- 297 to 919 +/- 375 pg/ml, p less than 0.05, and from 17 +/- 14 to 23 +/- 15 ng/ml/hr, p less than 0.05). Renal blood flow, urine output or sodium excretion did not change. Sodium output decreased at 1 hr from 6.9 mumol/min to 4.0 mumol/min, p less than 0.05. Both hepatic venous pressure gradient and azygos blood flow significantly increased by 21%. We conclude that the acute administration of fenoldopam did not improve renal hemodynamics or function in patients with cirrhosis and ascites. In addition, dopamine DA1 agonism caused further increases in norepinephrine concentration and plasma renin activity. Portal pressure also increased, probably because of an increase in mesenteric blood flow. These results question the renal benefit and raise concern about the use of dopamine agonists in patients with cirrhosis and ascites.
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PMID:Selective dopamine DA1 stimulation with fenoldopam in cirrhotic patients with ascites: a systemic, splanchnic and renal hemodynamic study. 167 Oct 29

Four pharmacons were tested on an acute portal pressure lowering effect in an experimental animal model with 25 normal and 25 rats with Thioacetamide-toxic liver cirrhosis. Invasive measurements of arterial and portal pressure were made under Hexobarbital-Sodium anaesthesia during 30 minutes after pharmacon application. The portal pressure of cirrhotic rats was under basic conditions 9.5 +/- 1.5 mm Hg and significant higher as in normal animals (5.3 +/- 0.9 mm Hg, p less than 0.01). After 10 mg/kg body mass Propranolol the portal pressure decreased in both animal groups small but not significantly over the whole measurement time. 1 mg/kg Verapamil lowered arterial middle pressure significantly, but increased portal pressure at all 15-20% in both animal groups. Application of 0.1 mg/kg Prazosin decreased the arterial middle pressure at all 5-15% and the portal pressure at all 20-30% in both study groups (both significantly). For Canrenoat-Potassium (20 mg/kg) no clear effect could by evaluated on portal pressure. The model of Thioacetamide-toxic cirrhosis of the rat offers conditions like cirrhosis in human medicine in order to study the effects of portal pressure lowering pharmacons. Propranolol and Prazosin decrease portal pressure and should by further investigated.
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PMID:[Pharmacological lowering of portal pressure in normal rats and in experimental liver cirrhosis]. 181 60

Recently it was suggested that the onset of sodium retention in experimental cirrhosis in rats is related to a critical threshold of hepatic function, as assessed by the aminopyrine breath test. The aim of this study was to evaluate whether sodium retention occurred after two-thirds hepatectomy in rats and to investigate the relationship between sodium retention and changes in hepatic function associated with liver regeneration in this model. Sodium balance, creatinine clearance, serum sodium and the aminopyrine rate constant of elimination were evaluated daily for 4 days after surgery in partially hepatectomized (n = 6) and sham-operated rats (n = 6). All rats in the partial hepatectomy group exhibited sodium retention (sodium balance greater than 0.7 mmol/day) 24 hr after surgery. This was associated with a 62% reduction of the aminopyrine rate constant of elimination. Spontaneous natriuresis which occurred between 2 and 4 days after surgery, was associated with an increase in the aminopyrine rate constant of elimination (from 0.73 +/- 0.02 x 10(-2) min-1 on the last day of sodium retention to 0.95 +/- 0.04 x 10(-2) min-1 on the first day of natriuresis [p less than 0.05]). In contrast, no change in creatinine clearance occurred over the same period. A negative curvilinear association was found between sodium balance and the aminopyrine rate constant of elimination in all animals (r = -0.72, p less than 0.001). These observations indicate that natriuresis is related to the recovery of liver function, not to changes in creatinine clearance. In conclusion, the concept of a critical threshold of liver function below which sodium retention occurs has been substantiated in this model of hepatic dysfunction.
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PMID:Sodium retention and hepatic function after two-thirds hepatectomy in the rat. 187 96

Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome, and pregnancy. Nonosmotic vasopressin release has been implicated in the water retention of these edematous disorders. The nonosmotic release of vasopressin is consistently associated with activation of the sympathetic nervous and renin-angiotensin-aldosterone systems in both experimental animals and in edematous patients. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin and activation of the renin-angiotensin system. These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. Neither total extracellular fluid volume nor blood volume is a determinant of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by a decrease in effective arterial blood volume (EABV) due to either a fall in cardiac output or peripheral arterial vasodilation. The acute response to a decrease in EABV involves vasoconstriction mediated by angiotensin, sympathetic mediators, and vasopressin. The slower response to restoring EABV involves vasopressin-mediated water retention and aldosterone-mediated sodium retention. The resultant renal vasoconstriction limits the distal tubular delivery of sodium and water, thus maximizing the water-retaining effect of vasopressin and impairing the normal escape from the sodium-retaining effects of aldosterone. The elevated glomerular filtration rate and filtered sodium load in pregnancy allows increased distal sodium and water delivery in spite of a decrease in EABV, thus limiting edema formation during gestation.
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PMID:Unifying hypothesis of sodium and water regulation in health and disease. 193 81

Twenty uncomplicated cases of cirrhosis of liver, proved by liver biopsy, and free from other systemic diseases were studied. Glucose (pre- and postprandial) and electrolytes (Na+, K+, Cl-) values were compared to those of systemic and portal venous blood. Chloride level in ascitic fluid was found to be significantly high in cirrhosis, as compared to portal and systemic venous blood. Sodium and glucose levels were similar in ascitic fluid and portal venous blood except in two cases complicated with tuberculous peritonitis, where pre- and postprandial glucose levels were considerably low. In 55% cases, there was impaired glucose tolerance, as measured by pre- and postprandial glucose levels in systemic venous blood.
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PMID:Study of ascitic fluid in relation to systemic and portal venous blood in hepatic cirrhosis. 194 Apr 16

Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome, and pregnancy. In recent years, the use of a sensitive radioimmunoassay for plasma vasopressin has implicated the role of nonosmotic vasopressin release in the water retention of these edematous disorders. In experimental studies and studies in man, it has been found that the nonosmotic release of vasopressin is consistently associated with the activation of the sympathetic nervous and renin-angiotensin-aldosterone systems. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin (carotid and aortic baroreceptors) and in the activation of the renin-angiotensin system (renal beta-adrenergic receptors). These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. In this context, neither total extracellular-fluid (ECF) volume nor blood volume are determinants of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by either a fall in cardiac output (e.g. ECF volume depletion, low-output cardiac failure, pericardial tamponade, or hypovolemic nephrotic syndrome) or peripheral arterial vasodilation (e.g. high-output cardiac failure, cirrhosis, pregnancy, sepsis, arteriovenous fistulae, and pharmacologic vasodilators). With a decrease in effective arterial blood volume (EABV). initiated by either a fall in cardiac output or peripheral arterial vasodilation, the acute response involves vasoconstriction mediated by angiotensin, sympathetic mediators, and vasopressin. The slower response to restoring EABV involves vasopressin-mediated water retention and aldosterone-mediated sodium retention. The renal vasoconstriction which accompanies those states that decrease EABV, by either decreasing cardiac output or causing peripheral arterial vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A unifying hypothesis of sodium and water regulation in health and disease. 210 96

Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome and pregnancy. In recent years the use of a sensitive radioimmunoassay for plasma vasopressin has implicated the role of nonosmotic vasopressin release in the water retention of these edematous disorders. In experimental studies and studies in humans it has been found that the nonosmotic release of vasopressin is consistently associated with activation of the sympathetic nervous and renin-angiotensin-aldosterone systems. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin (carotid and aortic baroreceptors) and activation of the renin-angiotensin system (renal beta-adrenergic receptors). These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. In this context neither total extracellular fluid (ECF) volume nor blood volume are determinants of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by either a fall in cardiac output (e.g. ECF volume depletion, low-output cardiac failure, pericardial tamponade or hypovolemic nephrotic syndrome) or peripheral arterial vasodilation (e.g. high-output cardiac failure, cirrhosis, pregnancy, sepsis, arteriovenous fistulae and pharmacologic vasodilators). With a decrease in effective arterial blood volume (EABV), initiated by either a fall in cardiac output or peripheral arterial vasodilation, the acute response involves vasoconstriction mediated by angiotensin, sympathetic mediators and vasopressin. The slower response to restoring EABV involves vasopressin-mediated water retention and aldosterone-mediated sodium retention. The renal vasoconstriction which accompanies those states that decrease EABV, by either decreasing cardiac output or causing peripheral arterial vasodilation, limits the distal tubular delivery of sodium and water thus maximizing the water-retaining effect of vasopressin and impairing the normal escape from the sodium-retaining effects of aldosterone. The elevated glomerular filtration rate and filtered sodium load in pregnancy allows increased distal sodium and water delivery in spite of a decrease in EABV, thus limiting edema formation during gestation.
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PMID:Pathophysiology of vasopressin in edematous disorders. 269 4


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