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

An oral water load of 20 ml kg-1 body weight was given to 11 patients with early hepatic cirrhosis and to 16 healthy control subjects. Urinary output (V), free water clearance (CH2O), urinary excretion of prostaglandin E2 (PGE2) and F2 alpha (PGF2 alpha), and plasma concentration of arginine vasopressin (AVP) were determined before and during the first 4 h after loading. During basal conditions, PGE2 excretion was the same in patients (75 pg min-1, median, range 15-569) and controls (78 pg min-1, range 22-262), but during the first hour after water loading, PGE2 increased to a significantly higher level in cirrhotic patients (423 pg min-1, median) than in control subjects (162 pg min-1) (P less than 0.05). No difference in PGF2 alpha excretion was found between the two groups. Urinary output and CH2O were significantly lower after water loading in patients than in controls. Arginine vasopressin before water loading did not differ between patients and control subjects, but after loading it was unchanged in the patients, whereas a significant reduction (1.9 to 1.4 pmol l-1, P less than 0.01) was found in the control subjects. In controls, but not in patients, PGE2 was significantly positively correlated to V and CH2O, and negatively correlated to AVP after water loading. Thus, renal PGE2 excretion is increased and CH2O is decreased after water loading in patients with early hepatic cirrhosis, and a disturbed relationship seems to exist between PGE2 on the one hand, and AVP and renal water excretion, on the other, in these patients after water loading.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disturbed relationship between urinary prostaglandin E2 excretion, plasma arginine vasopressin and renal water excretion after oral water loading in early hepatic cirrhosis. 313 26

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.
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PMID:Clinical and hormonal conditions associated with sodium retention in cirrhotic patients with ascites. Evaluation by univariate and multivariate analyses. 355 5

An oral water load of 20 ml per kg body weight was given to 9 patients with hepatic cirrhosis and 11 healthy controls. Urinary output, free water clearance, and plasma concentrations of arginine vasopressin, angiotensin II and aldosterone were determined before and three times during the first 4 h after loading. In the cirrhotic patients urinary output was significantly lower after loading than in the control subjects, mainly because of a lower free water clearance, and, in contrast to the healthy controls, the cirrhotic patients did not have natriuresis after water loading. No differences were found between patients and controls in arginine vasopressin, angiotensin II, aldosterone, or creatinine clearance. It is concluded that patients with well-compensated cirrhosis of the liver have an impaired ability to excrete sodium and water. This phenomenon does not seem to be due to increased arginine vasopressin secretion, activation of the renin-angiotensin-aldosterone system, or a decreased glomerular filtration rate.
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PMID:Impaired renal water excretion in early hepatic cirrhosis. Lack of relationship between renal water excretion and plasma levels of arginine vasopressin, angiotensin II, and aldosterone after water loading. 374 8

Hyperosmolality occurs when there are defects in the two major homeostatic mechanisms required for water balance-thirst and arginine vasopressin (AVP) release. In this situation hypotonic fluids are lost in substantial quantities causing depletion of both intracellular and extracellular fluid compartments. Patients with essential hypernatremia have defective osmotically stimulated AVP release and thirst but may have intact mechanisms for AVP release following hypovolemia. Hyperosmolality can also be seen in circumstances in which impermeable solutes are present in excessive quantities in extracellular fluid. Under these conditions there is cellular dehydration and the serum sodium may actually be reduced by water drawn out of cells along an osmotic gradient. Hyposmolality and hyponatremia may be seen in a variety of clinical conditions. Salt depletion, states in which edema occurs and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) may all produce severe dilution of body fluids resulting in serious neurologic disturbances. The differential diagnosis of these states is greatly facilitated by careful clinical assessment of extracellular fluid volume and by determination of urine sodium concentration. Treatment of the hyposmolar syndromes is contingent on the pathophysiology of the underlying disorder; hyponatremia due to salt depletion is treated with infusions of isotonic saline whereas mild hyponatremia in cirrhosis and ascites is best treated with water restriction. Severe symptomatic hyponatremia due to SIADH is treated with hypertonic saline therapy, sometimes in association with intravenous administration of furosemide. Less severe, chronic cases may be treated with dichlormethyltetracycline which blocks the action of AVP on the collecting duct.
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PMID:The clinical physiology of water metabolism. Part III: The water depletion (hyperosmolar) and water excess (hyposmolar) syndromes. 624 83

In a study of 26 patients with cirrhosis, plasma norepinephrine concentrations were significantly higher in 19 patients who abnormally excreted an acute water load than in seven who excreted the load normally (8324 +/- 116 vs. 306 +/- 33 pg per milliliter; P less than 0.001). There was also a significant positive correlation between plasma levels of norepinephrine and arginine vasopressin after the water load, as well as a negative correlation between plasma norepinephrine and the percentage of the load excreted. A positive correlation between plasma norepinephrine and plasma renin activity, as well as between norepinephrine and aldosterone, was observed. In addition, there was a negative correlation between plasma norepinephrine and urinary sodium excretion. These findings indicate that increased sympathetic activity, as assessed by plasma levels of norepinephrine, correlates closely with sodium and water retention in cirrhotic patients and thus may be of pathogenetic importance.
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PMID:Potential role of increased sympathetic activity in impaired sodium and water excretion in cirrhosis. 675 51

Twelve stable cirrhotic patients with ascites received a 20 mL/kg water load. Seven patients had abnormal water excretion (27.3% +/- 5.4% of the water load in 5 hours) and a minimal urine osmolality of 262 mosmol/kg water. Five patients excreted 82.6% in 5 hours and had a minimal urine osmolality of 65 mosmol/kg water. Mean plasma arginine vasopressin values after water load were significantly higher in Group 1 (1.34 +/- 0.36 pg/mL) than in Group 2 (undetectable). An effective blood volume lower in Group 1 than Group 2 patients was suggested by a lower plasma albumin (2.5 versus 3.3 g/dL, p less than 0.02), a higher pulse rate (96 versus 72, p less than 0.001), a higher plasma renin activity (7.8 versus 1.5 ng/mL . h, p less than 0.005), a higher plasma aldosterone (66 versus 21 ng/dL, p less than 0.05), and a lower urinary sodium excretion (2.7 versus 14.2 meq Na/5 h, p less than 0.005). The results suggest that nonosmotic stimulation of vasopressin secondary to a decrease in effective blood volume is an important factor in the abnormal water excretion of cirrhosis.
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PMID:Role of vasopressin in abnormal water excretion in cirrhotic patients. 706 56

The aim of this double-blind, placebo-controlled crossover study was to investigate the effect of 1-deamino-8-D-arginine vasopressin (dDAVP) on hemostasis in patients with chronic liver disease. Nine consecutive patients with biopsy-proven liver cirrhosis and related coagulation abnormalities received in a random order dDAVP, 0.5 microgram/kg, or saline intravenously. Blood samples were taken before dDAVP infusion and 30, 60 and 180 min after its end. dDAVP infusion induced a statistically significant shortening of the bleeding time from 9 min (range 6.5-15.5) to 6 min (range 4.5-9.5) at 1 h after the infusion. The activated partial thromboplastin time was significantly shortened at 30 and 60 min after dDAVP infusion. Plasma levels of factor VIII, XI and XII coagulant activities were significantly increased at all sampling times after dDAVP infusion. The maximum increase over basal values in plasma levels of factor VIII, XI and XII was 63, 22 and 40%, respectively. dDAVP did not induce any significant changes of prothrombin time, thrombin clotting time, fibrinogen, plasma levels of factor II, V, VII, IX, X, factor XII antigen, protein C (activity and antigen), antithrombin III, plasminogen and alpha 2-antiplasmin. Placebo infusion did not produce any significant changes in the evaluated parameters. We conclude that dDAVP can positively influence the hemostatic system in patients with liver cirrhosis. The clinical relevance of this hemostatic improvement deserves further evaluation.
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PMID:Effects of desmopressin on hemostasis in patients with liver cirrhosis. 748 63

Water retention is a complication in many patients with cirrhosis, usually attributed to excessive release of arginine vasopressin. To investigate the responsiveness of arginine vasopressin to osmotic and non-osmotic stimuli and its relationship to free water excretion, we studied 19 patients with cirrhosis under three different conditions: 45 min with legs raised to 60 degrees, to expand the central blood volume; infusion of 1000 ml of 0.45% saline solution to reduce plasma osmolality; and rapid injection of 50 ml of 2 M NaCl to increase plasma osmolality. Both expansion of central blood volume and decrease of plasma osmolality significantly reduced plasma vasopressin levels (from 2.1 +/- 0.6 to 1.39 +/- 0.3 pg/ml, p < 0.04; and from 1.09 +/- 0.25 to 0.41 +/- 0.13 pg/ml, p < 0.0001). The changes in free water excretion differentiated two subgroups of patients during each test: excretors and non-excretors. In the excretors, increased free water excretion was associated with suppressed vasopressin levels (below 0.5 pg/ml) and normal renal function. In the non-excretors, inability to improve free water excretion was associated with high vasopressin levels or with reduced distal delivery of the glomerular filtrate, except in some cases where vasopressin levels had fallen below 0.5 pg/ml and renal function was normal. For these cases the presence of other vasopressin-independent antidiuretic mechanisms is conceivable. The injection of hypertonic saline solution caused significant rises in plasma osmolality (from 287 +/- 1.9 to 292 +/- 1.6 mmol/kg, p < 0.05) and in plasma vasopressin levels (from 1.13 +/- 0.29 to 2.86 +/- 0.52 pg/ml, p < 0.05). These results suggest that vasopressin release in patients with cirrhosis is normally responsive to osmotic and non-osmotic stimuli, although our results show a lower theoretical osmolar threshold for suppression of vasopressin release in non-excretors than in excretors (276 vs 284 mmol/kg).
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PMID:Vasopressin release and water metabolism in patients with cirrhosis. 789 Aug 99

The present study was undertaken to determine whether a non-peptide arginine vasopressin (AVP) antagonist [5-dimethylamino-1-(4-(2-methylbenzoylamino)benzoyl]-2,3,4,5-tetra hydro-1H- benzazepine] (OPC-31260) improves the impaired water excretion in rats with experimental liver cirrhosis. Male Wistar rats weighing 200 to 250 g were injected in an equal volume (4 ml/kg) of carbon tetrachloride and olive oil at an interval of seven days for three months, causing liver cirrhosis with ascites. Control rats were injected with only olive oil. Body weight (body wt) and hematocrit (Hct) were lower in the cirrhotic rats than the control rats (body wt 360.7 vs. 238.5 g, P < 0.01; Hct 46.3 vs. 39.2%, P < 0.01). A water loading test (30 ml/kg) was carried out and 20-minute urine collections were made for three hours. The percent of water load excreted was 62.5% in the cirrhotic rats, a value significantly less than that of 102.1% in the control rats. However, its percent increased to 215.1% after the oral administration of 5 mg/kg OPC-31260 (P < 0.01). Minimal urinary osmolality (UOsm) was 185.5 mOsm/kg H2O in the cirrhotic rats receiving the vehicle, a value greater than the control rats of 125.5 mOsm/kg H2O (P < 0.01). The oral administration of 5 mg/kg OPC-31260 reduced minimal UOsm to 85.2 mOsm/kg H2O in the cirrhotic rats (P < 0.01). Urinary excretion of sodium was lower in the cirrhotic rats than the control rats (87.1 vs. 312.4 microEq/3 hr, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Therapeutic efficacy of the non-peptide AVP antagonist OPC-31260 in cirrhotic rats. 793 42

Taurine is a non-protein sulfur amino acid widely distributed in mammalian tissues, with poorly understood functions. Taurine administration has a variety of hemodynamic effects, including improvement of cardiac function and suppression of sympathetic activity. Increased urinary volume and sodium excretion have been reported in taurine-fed hamsters. Since patients with ascitic liver cirrhosis have severe hemodynamic and renal abnormalities potentially sensitive to taurine feeding, we evaluated the effects of the i.v. infusion of taurine on urinary flow and sodium excretion and on the hormones involved in the control of hydrosaline homeostasis. Eight cirrhotic patients with tense ascites were given an i.v. bolus of taurine (16 mumoles in 40 ml of saline). The next day patients were given saline only, as a control. Diuresis, urinary sodium and plasma renin activity, aldosterone, atrial natriuretic peptide and arginine vasopressin were measured for the following 6 hrs. Plasma taurine increased ten fold after infusion, then decreased exponentially. No side effects were recorded. After taurine, but not after saline, there was a prompt and significant increase in both urinary volume and sodium excretion. Diuresis increased from 340 +/- 43 to 817 +/- 116 microliters/min (p < 0.01); urinary sodium from 13.8 +/- 3 to 26.3 +/- 4 mumoles/min (p < 0.05). Both values returned to normal after 2-3 hrs. Taurine infusion caused a concomitant significant decrease in plasma renin activity (from 7.7 +/- 2.2 to 4.3 +/- 1.9 ng/ml/hr, p < 0.05) and aldosterone (from 588 +/- 47 to 348 +/- 89 pg/ml, p < 0.05), but no changes in atrial natriuretic peptide and arginine vasopressin. We conclude that i.v. taurine infusion in ascitic cirrhosis promotes a transient diuresis and natriuresis, apparently through the inhibition of the renin-aldosterone axis.
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PMID:Taurine-induced diuresis and natriuresis in cirrhotic patients with ascites. 819 77


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