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)

Two human neurophysins, nicotine stimulated neurophysin (NSN), and estrogen stimulated neurophysin (ESN) were assayed during physiologic maneuvers and pathologic states in man. NSN is thought to be associated with vasopressin and was elevated in some subjects by volume depletion, surgical stress, hypotension and hypertonic saline infusion. Overnight dehydration did not elevate NSN in spite of urinary concentration. NSN was elevated in some subjects with the syndrome of inappropriate secretion of antidiuretic hormone and when tested was unresponsive to administered water, alcohol or nicotine. ESN was elevated during estrogen administration, in pregnancy, in newborns and in patients with cirrhosis. NSN was also acutely increased at parturition. These data support the association of NSN with vasopressin although changes in NSN were found only with potent stimuli for vasopressin release. ESN may be associated with oxytocin but demonstration of this awaits knowledge of oxytocin physiology in humans.
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PMID:Physiologic control of two neurophysins in humans. 55 58

An acute volume expansion in water diuresis has been induced in 8 patients with liver cirrhosis and in 8 normal subjects, taken as controls. A two hour postinfusion urine sample has been utilized to obtain the urine fraction with natriuretic activity. This activity was assayed in 16 rats. Our results confirm a significantly lower natriuretic activity of cirrhotic urine fractions than those of controls.
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PMID:Sodium retention in chronic liver disease: lack of a natriuretic factor? 56 89

The RBF was measured by means of the 133Xe washout method in seventy patients with cirrhosis. The average RBF in controls was 3.72 ml/g-min compared with 2.34 in the patients without ascites, 1.82 in the decompensated patients, 1.47 in the patients with azotaemia and 1.13 in the patients with additional oliguria. The RBF was not significantly correlated to changes in the systemic or portal haemodynamics. Likewise it was not correlated to any biochemical test of liver function except the serum albumin concentration (P less than 0.01). From the present results it can be concluded that a reduction in RBF in cirrhosis frequently is present before sodium and water retention is clinically evident and before laboratory proof of impairment of renal function, and that a subnormal serum albumin concentration may be a factor among several leading to renal hypoperfusion in cirrhosis.
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PMID:Renal blood flow in cirrhosis: relation to systemic and portal haemodynamics and liver function. 59 43

Fluid retention and ascites are rarely seen in patients with primary biliary cirrhosis (PBC). This contrasts with the conspicuous tendency of patients with Laennec's cirrhosis to retain salt and water. In an attempt to clarify this clinical observation, renal handling of sodium was studied during extracellular volume expansion (ECVE) and maximal suppression of antidiuretic hormone in five patients with PBC. These PBC patients were compared with two control populations: five edema-free patients with Laennec's cirrhosis and nine healthy volunteers. The natriuretic and diuretic response to ECVE was significantly greater in the patients with PBC as compared with the two control groups. CH2O for given rates of urine flow were similar in PBC patients as compared with normal subjects. The data suggest that a supranormal rejection of sodium at the proximal tubule in response to ECVE underlies the exaggerated natriuresis of PBC. The augmented elimination of salt during ECVE in patients with PBC may explain the rarity of ascites and edema in this variety of cirrhosis.
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PMID:Exaggerated natriuretic response to volume expansion in patients with primary biliary cirrhosis. 60 57

Renal handling of sodium was studied in five dogs where an end-to-side portacaval fistula was constructed prior to the induction of cirrhosis with DMN. Such a model permits the effects of cirrhosis to be studied separately from the consequences of portal hypertension. Three control animals without cirrhosis maintained normal liver and kidney function and remained in sodium balance for as long as 8 weeks following surgery. In the five cirrhotic dogs, urinary sodium retention preceded ascites formation and was independent of hyperaldosteronism, hypoalbuminemia, hepatic ischemia, or decreased renal perfusion. Portal venous pressure remained normal in all cirrhotic dogs, and the splanchnic area remained free of venous collaterals. Plasma volume expansion also preceded ascites formation, and this variable increased by 8.4% (p less than 0.05) following 6 days of sodium retention. These temporal relationships between sodium retention, expanded plasma volume, and ascites formation are similar to those observed in ordinary cirrhotic dogs previously studied in this laboratory. Total plasma volume increased by 13.2% (p less than 0.05) when measured during the ascitic phase of cirrhosis. However, when the splanchnic and nonsplanchnic ("effective") components of plasma volume were measured by an exclusion technique, the ratio of these components to total plasma volume was not different from that observed in normal dogs. Thus no preferential consignment of retained salt and water had occurred. We conclude that urinary sodium retention in cirrhotic dogs occurs independently of portal hypertension or augmented splanchnic vascular capacity and is associated with expansion of the effective plasma volume, even though ascites is present.
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PMID:Renal sodium retention and ascites formation in dogs with experimental cirrhosis but without portal hypertension or increased splanchnic vascular capacity. 62 53

Twelve patients with cirrhosis, refractory ascites, and varying degrees of renal failure (creatinine clearance, 5 to 44 ml/min) were studied before and up to 2 weeks following peritoneovenous shunt. Creatinine clearance increased 60% or more in seven patients (group I) and 22% or less in five patients (group II). There were no significant differences in maximum urine output or sodium excretion between groups (group I, 4,272 ml/14 hr, 372 mEq/24 hr; group II, 3,722 ml/24 hr, 255 mEq/24 hr). Aldosterone and renin concentrations were higher in group I and showed a greater decrease after shunting. Renin substrate levels also were higher in group I and rose following shunt insertion, while group II remained low. Ascitic fluid was found to contain renin substrate in concentrations of approximately 25% to 50% of plasma concentrations. Patients with the greatest increase in creatinine clearance showed the largest rise in substrate concentration and fall in renin and aldosterone secretion, suggesting a dynamic relationship between these factors. That a diuresis could occur without significant change in these parameters in five of 12 patients suggests independent control mechanisms for renal salt and water excretion and glomerular filtration in the ascitic patient.
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PMID:Improved renal function and inhibition of renin and aldosterone secretion following peritoneovenous (LeVeen) shunt. 66 20

Mobilization of ascites was studied in 20 anesthetized dogs with experimental cirrhosis following a mannitol- or furosemide-induced diuresis. Observations were made at 2 h following the drug, at which time the diuresis was invariably completed, and repeated at 4 h following a 2-h recovery period, during which the ureters were clamped to prevent further urinary losses. In the furosemide group the mean urinary loss was 459 +/- 6 ml and was accompanied by a decline in central venous pressure and hemoconcentration. At 2 h plasma volume had declined by 14% from control values, but at 4 h plasma replenishment was 99% complete. At this time ascites volume had decreased by 467 ml, acting as the major source for vascular replenishment. In the mannitol group, the average urinary loss was 190 +/- 10 ml and was accompanied by maintenance of venous pressure, lack of hemoconcentration, and hyponatremia. At 2 h plasma volume had expanded from control values by 22%, but at 4 h vascular replenishment was only 78% complete. The average ascites volume had decreased by only 55% of the diuretic loss, and was mobilized by a complex sequence of events involving movement of intracellular water.
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PMID:Mobilization of ascites in cirrhotic dogs following furosemide or mannitol diuresis. 67 15

Proximal tubular reabsorption was examined in patients with liver cirrhosis and ascites by a variety of indirect methods. Maximal diluting ability, urine flow rate, and free water clearance were reduced. During frusemide administration V/GFR was lower than in normal control subjects, indicating that proximal fractional reabsorption is enhanced in liver cirrhosis. This, by reducing Na delivery to the loop of Henle, impairs maximal urine osmolality. Mannitol, by reducing proximal reabsorption, restores availability of Na to the loop and urine concentrating ability during osmotic diuresis, whereas volume expansion with dextran was ineffective. This could be due to a persistent increase in renal vascular resistance preventing the rise in interstitial pressure responsible for driving fluid back into the proximal tubular lumen.
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PMID:Reabsorption of sodium in the proximal renal tubule in cirrhosis of the liver. 68 May 84

The intracellular sodium, potassium, and water content of isolated leucocytes was estimated in 47 patients with cirrhosis. The values for sodium showed a wide scatter. In patients without ascites the mean value was significantly increased but in those accumulating ascites it was normal, although often reduced in individual subjects. Reduced values were found in patients with hyponatraemia associated with end-stage cirrhosis and diuretic treatment. Changes in leucocyte water content closely followed those in sodium content. Leucocyte potassium content was normal except in patients accumulating ascites in whom it was significantly reduced, indicating whole body depletion, and this could be corrected by administration of spironolactone.
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PMID:Changes in the electrolyte content of leucocytes at different clinical stages of cirrhosis. 68 May 96

Thioacetamide-fed rats developed cirrhosis with portal hypertension (P portal=23.0 +/- 5.2 cm H2O, controls: 14.4 +/- 1.0 cm H2O). The PO2 of liver tissue was markedly reduced in cirrhosis (PO2=7.6 +/- 3.4 torr, controls 22.3 +/- 5.8 torr), and the aortal pH was significantly lower as well. No correlation was found between portal hypertension, development of large--nodular cirrhosis, and ascites.
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PMID:Hemodynamic parameters and blood gas analyses in the normal and the cirrhotic rat. 68 97


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