Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma levels of atrial natriuretic factor (ANP) were examined in 12 patients with liver cirrhosis (6 with ascites) and 6 controls before and after the administration of the infusion of 2000 ml of saline solution per 70 kg of body weight during 2 hours. Basal concentration of ANF tended to be slightly, but nonsignificantly higher in patients with ascitic liver cirrhosis (5.5 +/- 1.3 fmol/ml) than in controls (3.0 +/- 1.0 fmol/ml) and in patients with non-ascitic liver cirrhosis (4.6 +/- 1.3 fmol/ml). Saline administration led to the comparable increase of plasma ANF in ascitic (14.2 +/- 4.0 fmol/ml) and non-ascitic cirrhotics (15.7 +/- 3.7 fmol/ml) and in controls (12.4 +/- 4.3 fmol/ml). The increase of plasma ANF was accompanied by the suppression of plasma renin activity (PRA) and plasma aldosterone (PA) in all groups; in ascitic patients, however, PRA and PA remained above the normal range. While in controls and non-ascitic cirrhotics saline administration led to the increase of urine flow rate /from 0.74 +/- 0.13 to 2.04 +/- 0.44 ml/min, P less than 0.01, in controls; from 0.83 +/- 0.05 to 1.28 +/- 0.07 ml/min, P less than 0.01, in non-ascitic cirrhotics) and urinary sodium excretion (from 110.7 +/- 21.3 to 364.8 +/- 74.4 umol/min, P less than 0.01, in controls; from 125.0 +/- 16.7 to 218.7 +/- 24.3 umol/min, P less than 0.01 in non-ascitic cirrhotics), in patients with ascitic liver cirrhosis neither urine flow rate (from 0.66 +/- 0.1 to 0.72 +/- 0.15 ml/min, n.s.), nor urinary sodium excretion (from 16.7 +/- 9.9 to 54.2 +/- 40.3 umol/min, n.s.) changed significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic factor in liver cirrhosis--the influence of volume expansion. 253 Nov 15

The renal response to atrial natriuretic factor (ANF) (175 ng.kg-1.min-1) was tested in nine dogs during a control period and again after the appearance of experimental cirrhosis, ascites, and avid sodium retention. During the cirrhotic phase, plasma volume had increased by 28.4% (P less than 0.05), renal perfusion and glomerular filtration rate (GFR) were unchanged from control values, and plasma immunoreactive ANF (iANF) had declined from 71.6 +/- 9.5 to 34.7 +/- 5.4 pg/ml (P less than 0.05). During the control phase, change of urinary sodium excretion rate (delta UNaV) increased by 132 +/- 22 mu eq/min but was attenuated in the cirrhotic phase (delta UNaV = 29 +/- 12.5 mu eq/min). Of these nine cirrhotic dogs, five responded with a delta UNaV ranging from 20 to 114 mueq/min (mean delta UNaV = 59.6 +/- 10.6 mu eq/min), whereas 4 were nonresponders (delta UNaV = 1.3 +/- 0.6 mu eq/min). In neither group could delta UNaV be correlated to changes in GFR, clearance of p-aminohippurate, or filtration fraction. In an additional 10 dogs studied only during cirrhosis, 5 were natriuretic responders and 5 were nonresponders. Atrial content of ANF, half time of infused ANF, and plasma levels of iANF did not differentiate the two groups. We conclude that, like chronic caval dogs with ascites, salt-retaining cirrhotic dogs show heterogeneity of natriuretic response to infused ANF, which is unexplained by differences in renal perfusion.
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PMID:Heterogeneous renal responses to atrial natriuretic factor. II. Cirrhotic dogs. 253 53

Atrial natriuretic factor (ANF), a recently sequenced cardiac peptide, has been shown to have potent natriuretic, diuretic, and vasodilating effects in several species. We have developed a radioimmunoassay to measure the levels of immunoreactive ANF in human plasma. Plasma levels of ANF in healthy volunteers on a low sodium diet were 9.8 +/- 1.4 pmol/liter and increased to 21.9 +/- 3.0 on a high sodium diet. The levels of atrial natriuretic factor correlated directly with urinary sodium and inversely with plasma renin activity and plasma aldosterone levels. Patients with marked edema due to congestive heart failure had plasma levels of atrial natriuretic factor five times higher than normal (P less than 0.05), whereas patients with cirrhosis and edema had levels that were not different from normal. These results suggest that atrial natriuretic factor plays an important role in the adaptation to increased sodium intake.
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PMID:Plasma levels of immunoreactive atrial natriuretic factor in healthy subjects and in patients with edema. 293 71

The present study was designed to investigate whether cirrhosis with ascites is associated with altered tissue content of atrial natriuretic factor. Atrial extracts from 14 cirrhotic rats with ascites and increased plasma renin activity (PRA) (14.4 +/- 4.6 ng X ml-1 X h-1) and aldosterone concentration (148.3 +/- 17.3 ng/dl) and from 10 control rats (PRA, 3 +/- 0.5 ng X ml-1 X h-1; aldosterone, 34.7 +/- 3.7 ng/dl) were intravenously injected into anesthetized normovolemic rats. Only one extract was assayed in each bioassay rat. Atrial extracts from control rats increased diuresis and natriuresis 513 +/- 91 and 3,029 +/- 752%, respectively (means +/- SE). In contrast, atrial extracts from cirrhotic rats increased urine volume 199 +/- 49% (P less than 0.001) and sodium excretion 546 +/- 132% (P less than 0.001). These results strongly suggest that atrial content of atrial natriuretic factor is reduced in cirrhotic rats as compared with control animals.
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PMID:Atrial natriuretic factor: reduced cardiac content in cirrhotic rats with ascites. 293 85

Since the discovery of the atrial natriuretic factor (ANF) an endocrine function has been attributed to the mammalian heart. This function may include definition of optimal conditions for efficient performance of the heart, e.g. by reduction of afterload in hypertension or of preload and afterload in heart failure. Plasma ANF levels were measured in various cardiovascular disease states and compared with those of controls and of patients with liver cirrhosis. Plasma ANF levels in hypertensive patients were sevenfold higher than in controls, and in patients with heart failure 40-fold higher than normal values. Small differences were detected between controls and patients with cirrhosis of the liver, in spite of the impaired renal sodium handling seen in cirrhotics. Plasma ANF levels were significantly correlated with haemodynamic parameters and were inversely related to the cardiac index. Treatment with an angiotensin converting enzyme inhibitor led to a significant decrease in plasma ANF levels in parallel with the haemodynamic improvement. Preliminary chromatographic analysis suggested differences in the structure of plasma ANF between normotensive and hypertensive subjects.
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PMID:Atrial natriuretic factor in plasma of patients with arterial hypertension, heart failure or cirrhosis of the liver. 294 36

This review examines current understanding about the patient with moderately advanced cirrhosis of the liver and his or her transition to hepatorenal syndrome (HRS). Special emphasis is given to three areas of ongoing research. Atrial natriuretic factor's role in the pathogenesis of salt and water retention is examined, as well as its role in determining volume status in these patients. The current literature regarding prostaglandins (PGs) is reviewed, with emphasis on how vasodilatory PGs appear first to help maintain homeostasis in advanced cirrhosis and how vasoconstrictor thromboxane may then be involved in the transition to HRS. Finally, new findings regarding the liver hormone glomerulopressin are examined, and how deficient release of this may lead to the decrease in glomerular filtration rate seen in HRS.
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PMID:Pathogenesis of the hepatorenal syndrome. 295 1

Atrial natriuretic peptide(s) (ANP), are thought to be released from the cardiac atria in response to distension. If decreased effective circulating blood volume is important in pathogenesis of ascites, plasma ANP levels would be expected to be decreased in ascitic subjects because of decreased atrial distension. To test this hypothesis, we measured plasma ANP by competitive radioimmunoassay in three groups of fasted, supine hospitalized subjects: nine noncirrhotic control subjects, 12 cirrhotics without ascites, and 17 cirrhotics with moderate to marked ascites. Immunoreactive plasma ANP concentrations were 195 +/- 41, 171 +/- 31, and 137 +/- 34 pg/ml (m +/- SD), respectively, in the three groups. The mean concentration in the group with cirrhosis and ascites was significantly (p less than or equal to 0.01) les than those of the other two groups, which did not differ from one another. These results support the concept that decreased effective circulating volume plays a role in pathogenesis of cirrhotic ascites, and that a relative deficiency of ANP plays a role in the sodium retention of decompensated cirrhosis.
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PMID:Plasma concentrations of immunoreactive atrial natriuretic peptide in hospitalized cirrhotic and noncirrhotic patients: evidence for a role of deficient atrial natriuretic peptide in pathogenesis of cirrhotic ascites. 252 1

The aim of this study was to determine the plasma levels, cardiac release and splanchnic extraction of atrial natriuretic factor in cirrhosis with ascites. The plasma concentration of immunoreactive atrial natriuretic factor in samples obtained from an antecubital vein was measured in 18 healthy volunteers and in 35 cirrhotics with ascites. In 11 of these cirrhotics and in 11 patients admitted to the hospital for the study of a thoracic pain who had no clinical or hemodynamic signs of cardiac failure (control group), the plasma levels of immunoreactive atrial natriuretic factor in samples from the coronary sinus, right atrium, pulmonary artery, hepatic vein and femoral vein were determined and the coronary sinus blood flow measured by thermodilution. Cirrhotic patients showed significantly higher plasma levels of immunoreactive atrial natriuretic factor in each vascular territory studied than did control subjects (coronary sinus: 101.2 +/- 10.6 vs. 26.1 +/- 4.7 fmoles per ml; right atrium: 32.5 +/- 5.8 vs. 9.4 +/- 3.5; pulmonary artery: 36.8 +/- 10.1 vs. 7.5 +/- 2.4; hepatic vein: 10.7 +/- 2.0 vs. 2.7 +/- 0.8; femoral vein: 18.2 +/- 2.4 vs. 3.1 +/- 0.9; antecubital vein: 14.7 +/- 1.6 vs. 4.0 +/- 0.8). The coronary sinus blood flow was also higher in cirrhotics (200 + 22 ml per min) than in controls (105 +/- 7 ml per min). Consequently, the estimated cardiac release and cardiac production of immunoreactive atrial natriuretic factor were strikingly increased in cirrhotics (13,334 +/- 2,007 and 5,484 +/- 1,734 fmoles per min, respectively) as compared to control subjects (1,669 +/- 338 and 1,431 +/- 350 fmoles per min, respectively; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic factor in cirrhosis with ascites: plasma levels, cardiac release and splanchnic extraction. 252 73

Functional renal failure of cirrhosis (FRFC) is a usually fatal syndrome of acute renal failure occurring in patients with advanced liver disease. Although not conclusively proven, most evidence suggests that renal arterial and arteriolar vasoconstriction is the cause of the renal failure in these patients. However, the mediators of the vasoconstriction remain unknown. Human atrial natriuretic factor (hANF) is a hormone with potent natriuretic, diuretic, and vasorelaxant properties. A deficiency of hANF could lead to renal arterial vasoconstriction and avid renal sodium retention as seen in FRFC. This study was undertaken to determine if patients with FRFC are deficient in circulating hANF. Seven patients with advanced alcoholic liver disease and renal failure of unknown cause (FRFC) were compared with 7 patients with advanced alcoholic liver disease, ascites, and normal serum creatinine as well as with 14 healthy volunteers. Plasma hANF was measured by radioimmunoassay. Plasma hANF was 742 +/- 227 pg/ml (mean +/- SEM) in patients with FRFC compared with 360 +/- 70 pg/ml in patients with liver disease and normal serum creatinine (p greater than 0.05) and 28 +/- 5.7 pg/ml in healthy volunteers (p less than 0.005 vs. FRFC and chronic liver disease, ascites, and normal serum creatinine). Thus, FRFC is not caused by a deficiency of circulating hANF. The elevated plasma hANF levels in patients with chronic liver disease and continued sodium retention may suggest a renal insensitivity to the natriuretic effects of hANF.
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PMID:Plasma human atrial natriuretic factor in cirrhosis and ascites with and without functional renal failure. 297 83

Presence of atrial natriuretic factor (ANF)-like material was demonstrated by radioimmunoassay in ascitic fluid of 14 patients with cirrhosis of the liver. Immunoreactive ANF concentrations (M +/- SEM) were 2.4 +/- 0.5 fmol/ml in ascites, significantly lower (p less than 0.001) than the corresponding plasma concentrations of 15.5 +/- 2.6 fmol/ml. High performance gel permeation chromatography and reverse phase high performance chromatography of the ascitic ANF immunoreactivity showed correspondence to the alpha human ANF (99-126). ANF levels in ascites were significantly (p less than 0.01) correlated to levels in plasma (r = 0.66).
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PMID:Presence of the atrial natriuretic factor (ANF) in human ascitic fluid. 297 44


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