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

Basing on our supposition that "humoral mechanism" played an important role in the pathogenesis of portal hypertension due to cirrhosis, antagonists to some of these humoral substances (HS) would have a lowering effect on the portal pressure in cirrhotic patients. The wedged hepatic venous pressure (WHVP) was used as an indicator in reflecting the changes of portal pressure. Cimetidine was given intravenously to 8 cirrhotic patients, an average lowering of 0.72 kPa (7.3 cm H2O) of WHVP was observed. This was of clinical significance as compared with the previous results of splenorenal shunting operations.
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PMID:[Effect of cimetidine on wedged hepatic venous pressure in cirrhotic patients]. 181 46

The potent diuretic and natriuretic properties of atrial natriuretic factor (ANF) suggest that atrial hormones may participate to the regulation of salt and water excretion under physiological conditions. ANF, via the increase of its intracellular second messenger cGMP, has been recently shown to inhibit the apical sodium channel of the inner medullary collecting tubule (IMCD). In addition, ANF inhibits renin and aldosterone synthesis and antagonizes the antinatriuretic effects of angiotensin II. ANF may also contribute to the excretion of free water by inhibiting both the secretion of vasopressin and its antidiuretic action. ANF appears to play an important physiological role in sodium repleted states, or when the effective plasma volume is increased. On the contrary, when the effective plasma volume is decreased or in sodium depleted states, the natriuretic effect of both endogenous and exogenous ANF is severely blunted. That ANF-resistance may be related to the activation of the renin-angiotensin-aldosterone axis, increased circulating catecholamines, renal sympathetic nerve stimulation, changes in renal hemodynamics or increased degradation of ANF. All these factors could explain the lack of significant natriuretic effect of both endogenous and exogenous ANF in some pathological conditions such as heart failure or liver cirrhosis. ANF may also been concerned in water homeostasis. In addition to the well-known osmoregulatory pathways of water metabolism, we recently found that ANF could be involved in the volume adjustment to acute water intake in normal man.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic factor and the endocrine control of electrolyte homeostasis. 183 42

Cardiac atria and, under certain circumstances, also ventricles produce and secrete into the circulation atrial natriuretic factor (ANF). ANF exerts a significantly natriuretic, myorelaxant, renin-, aldosterone-, and vasopressin-inhibiting effect and acts as a neurotransmitter in the central and autonomous nervous systems. Expansion of the extracellular volume stimulates secretion of ANF which consequently contributes to renal excretion of sodium and water. The renal effect of ANF is apparently modulated by interaction with other mechanisms. ANF concentration in peripheral blood is the product of its secretion by the heart and degradation by peripheral tissues. In ascitic liver cirrhosis, the decreased splanchnic bed uptake may contribute to the increase in plasma ANF concentration observed. Insufficient production or secretion of ANF are not likely to be the primary etiopathogenic mechanism of arterial hypertension. In the course of development of hypertension, ANF is mobilized as a corrective-adaptive mechanism in an effort to normalize the raised BP, extracellular volume or circulating pressor agents. Through its production of ANF, the heart possess an important endocrine function markedly affecting pressure, electrolyte and volume homeostasis.
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PMID:Role of the heart as an endocrine organ. 184 37

The RAS is part of an extremely powerful feedback system for long-term control of blood pressure and volume homeostasis. Disturbances that tend to lower blood pressure, such as heart failure, cirrhosis, and peripheral vasodilation, cause sodium and water retention until blood pressure returns to normal due, in large part, to the combined actions of ANGII and reduced arterial pressure. In response to increased sodium intake, decreased ANGII formation greatly amplifies the effectiveness of pressure natriuresis, thereby preventing large increases in body fluid volumes and blood pressure. In circumstances in which the RAS is inappropriately activated, the sodium retaining effects of ANGII necessitate increased blood pressure to maintain sodium balance via pressure natriuresis. Because the RAS is so powerful in regulating blood pressure, blockade of the system with ACE inhibitors offers a powerful therapeutic tool in diseases such as hypertension and congestive heart failure. The control of sodium excretion and blood pressure by ANGII is exerted through multiple intrarenal as well as extrarenal effects, including stimulation of aldosterone secretion, which can influence renal excretion. Current evidence suggests that the intrarenal effects of ANGII are quantitatively more important than those mediated by aldosterone in controlling blood pressure and renal excretion. The most important intrarenal effects of ANGII include efferent arteriolar constriction as well as direct effects on sodium transport. The constrictor effect on efferent arterioles also is important in preventing reductions in GFR in circumstances associated with impaired renal perfusion. Therefore blockade of ANGII formation in circumstances such as renal artery stenosis may caused marked reductions in GFR. However, in many patients efferent arteriolar vasodilation caused by ANGII blockade may not lower GFR markedly because of other autoregulatory mechanisms that compensate by causing parallel reductions in afferent arteriolar resistance. In these individuals, chronic ACE inhibition may prove to be beneficial in slowing the progression of renal disease because a reduction in glomerular hydrostatic pressure may help to prevent glomerular damage.
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PMID:The renin-angiotensin system: renal actions and blood pressure regulation. 187 29

Various 4-arylthiomethyl-2-oxo-1,3-dioxole derivatives IIIa-o were synthesized. Their hydrolysis rates by arylesterase (EC 3.1.1.2) and cholinesterase (EC 3.1.1.8) in human serum were evaluated. Some of them were not hydrolyzed by cholinesterase, but were hydrolyzed easily by arylesterase. Among the substrates, sodium 4-((5-methyl-2-oxo-1,3-dioxol-4-yl)methylthio)benzenesulfonate (IIIg) was selected for its substrate reactivity toward arylesterase and its good water solubility. In addition, neither aliesterase (EC 3.1.1.1), acetylesterase (EC 3.1.1.6) nor cholesterol esterase (EC 3.1.1.13) hydrolyzed the compound. IIIg is thus concluded to be a specific substrate for arylesterase. Our assay system for serum arylesterase using IIIg can be readily applied to an automatic analyzer in the diagnosis of liver cirrhosis.
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PMID:2-Oxo-1,3-dioxoles as specific substrates for measurement of arylesterase activity. 193 62

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

Endogenous opioids may be involved in the pathogenesis of ascites and edema in patients with liver cirrhosis. We administered the opioid antagonist naloxone (5 mg bolus followed by a 0.06 mg/min infusion) to eight male patients with alcoholic cirrhosis and ascites and to five healthy age- and sex-matched control subjects and determined the effects of naloxone on water and electrolyte excretion after a nonsustained water load (20 ml/kg). In comparison with saline vehicle infusion carried out in the same subjects, naloxone administration resulted in a 50% increase in urine output and creatinine clearance and twofold increases in sodium and potassium excretion in patients with cirrhosis. Fractional sodium and potassium excretion, minimal urinary osmolality, plasma vasopressin and aldosterone levels, arterial blood pressure, and heart rate were not affected by naloxone treatment. The diuretic effect of naloxone was not observed in control subjects. Plasma naloxone levels were about six times higher in patients with cirrhosis than in control subjects (probably because of impaired metabolism of the drug) but only a weak correlation was found between drug levels and the degree of diuresis observed. The diuretic effect of naloxone may be related to an increase in glomerular filtration rate, possibly in conjunction with altered tubular reabsorption.
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PMID:Naloxone increases water and electrolyte excretion after water loading in patients with cirrhosis and ascites. 194 May 89

Using H2[18O] tracer isotope dilution and corrected bromide space as standard reference techniques, we determined total body water and extracellular water in cirrhotic patients with (four men and four women) and without (seven men and six women) ascites and compared them with a normal control group (eight men and six women). These results were then compared with calculations of total body and extracellular water determined by the bioelectrical impedance analysis technique. According to H2[18(O)] dilution, total body water was similar in cirrhotic patients without ascites and in controls (60.8% +/- 2.1% vs. 60.3% +/- 1.4% body wt), but was increased in patients with ascites (69.7% +/- 1.2% body wt; p less than 0.002). Correlation was excellent between the H2[18(O)] dilution and bioelectrical impedance measurements of total body water in controls and cirrhotic patients without ascites (r = 0.98; p less than 0.0001). However, this correlation was poor in cirrhotic patients with ascites (r = 0.17; not significant). According to the bromide space, extracellular water (expressed as a percentage of total body water) was increased in cirrhotic patients with (57.8% +/- 1.8%; p less than 0.001) and without (44.0% +/- 1.2%; p less than 0.001) ascites compared with controls (36.6% +/- 1.0%). A poor correlation (r = 0.41; p less than 0.13) was seen for extracellular water measurements between the bromide space method and the bioelectrical impedance method, which failed to detect the differences among the three groups observed with the bromide space technique. Furthermore, bioelectrical impedance failed to detect any change in total body or extracellular water after paracentesis, with a degree of inaccuracy that increased linearly as the amount of ascitic fluid removed increased (r = 0.97; p less than 0.001). All these intergroup comparisons remained the same, whether the analysis was of both men and women combined or for each gender individually. However, we saw differences between men and women in the control group and cirrhotic group without ascites. These results demonstrate that abnormalities in water homeostasis and compartmentalization between intracellular (the difference between total body and extracellular water fluid) and extracellular water may exist in cirrhosis whether or not fluid accumulation is clinically evident. These data further indicate that alterations in the metabolically active body cell mass (as represented by intracellular water) in cirrhosis may occur independently of total body water and calculated fat-free body mass. In addition, gender is an important variable to control for in studies of this type.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Measurements of total body and extracellular water in cirrhotic patients with and without ascites. 195 61

Plasma concentrations of atrial natriuretic factor (ANF) and cyclic 3',5'-guanosine monophosphate (cGMP) were measured in 11 cirrhotic patients with ascites, 11 cirrhotic patients without ascites and 15 control subjects. The following were determined in 15 of the cirrhotic patients and in all the control subjects: blood volume (BV) and furosemide-induced changes in BV, plasma values of ANF, cGMP, angiotensin II (AII), aldosterone (Aldo), arginine vasopressin (AVP) and urinary excretion rates of cGMP, prostaglandin E2 (PGE2), water and sodium. Basal plasma levels of ANF and cGMP were higher in patients with cirrhosis than in controls, but were the same in both groups of cirrhotics (ANF: cirrhosis with ascites 12.7, without ascites 13.4, and in controls 5.8 pmol l-1 (medians); cGMP: 7.7, 7.4 and 4.3 nmol l-1, respectively). BV was less reduced after furosemide in the cirrhotic patients (6.0%) than in the healthy subjects (10.1%), but basal BV did not differ. Urinary sodium excretion rates after furosemide were significantly lower in the cirrhotic patients than in the controls. PGE2 excretion rate increased after furosemide in the cirrhotic patients (0.29 to 0.66 pmol min-1; P less than 0.01) but not in the controls (0.31 to 0.38 pmol min-1). After furosemide ANF and cGMP decreased slightly in both groups whereas AII and Aldo increased; AVP increased in the controls, but not in the cirrhotic patients. In conclusion, plasma values of ANF and cGMP are increased in liver cirrhosis both with and without ascites. This and the elevated PGE2 excretion after furosemide may be compensatory phenomena in order to facilitate renal sodium excretion.
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PMID:Atrial natriuretic factor, cyclic 3',5'-guanosine monophosphate and prostaglandin E2 in liver cirrhosis: relation to blood volume and changes in blood volume after furosemide. 196 25

Ten patients with chronic hepatic disease (CHD) were compared with 34 non-CHD (N) pts. All patients underwent a peritoneal equilibration test; the asymptotic curves for small solutes transport were transformed into straight lines; protein transport was also expressed as a straight line; the slopes of these linear functions were used as index of solute transfer. CHD patients showed increased UF and transport of all solutes. The well-known relationships between UF and glucose absorption and between UF and dialysate sodium concentration were observed in N, but not in CHD patients. In patients without hepatic disease there was also a relationship between UF and the glucose transport slope, which was not observed in CHD pts. These results are probably due to the influence of hepatic lymph production plus increased lymphatic removal, observed in non uremic patients affected by cirrhosis, on the mechanisms of water and solute transport in CAPD. CHD patients can be managed either with CAPD or with short frequent exchanges. Ascites production can be evaluated by the difference between the observed UF in a patient with CHD and the expected UF in N patients.
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PMID:Transport of water and solutes in uremic patients with chronic hepatic disease in CAPD. 198 13


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