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 and 24-h urinary adenosine 3':5'-monophosphate (cyclic AMP) and guanosine 3':5'-monophosphate (cyclic GMP) were measured by radioimmunoassay in 12 normal subjects, 33 patients with six types of non-neoplastic disease (cholelithiasis, peptic ulcer, coronary heart disease, hypertension, regional ileitis, and cirrhosis), and 34 patients with five types of disseminated neoplastic disease (acute myelocytic leukemia; Hodgkin's disease; and metastatic cancer of the lung, colon, and breast). In patients with non-neoplastic disease, cyclic nucleotide values in plasma and urine did not differ significantly (P greater than 0.05) from those in normal subjects. In patients with disseminated cancer, cyclic AMP values in plasma and urine likewise did not differ significantly from those in normal subjects. Plasma cyclic GMP, in contrast, was significantly elevated in all five types of cancer patients, and urinary cyclic GMP was significantly elevated (five times the normal mean) in patients with acute myelogenous leukemia and Hodgkin's disease.
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PMID:Plasma and urine cyclic guanosine 3':5'-monophosphate in disseminated cancer. 22 52

Plasma and 24-hour urinary cyclic AMP and cyclic GMP levels were determined by saturation analysis in specimens from normal subjects and from 101 patients with tumours of the gastrointestinal tract, breast, lung, bladder or prostate, or with cirrhosis of the liver. Relative to 46 control subjects, plasma cyclic GMP concentrations were significantly elevated in seven patients with gastric tumours, 20 patients with cancer of the breast, six patients with lung cancer, and 12 patients with cirrhosis of the liver. Urinary cyclic GMP/creatinine ratios were significantly increased in cirrhotic patients and in the lung and oesophageal cancer groups. In no cancer group were increases in plasma or urine cyclic GMP levels sufficiently consistent to be of value in the diagnosis of human malignant disease. Changes in extracellular fluid cyclic nucleotide levels in the cirrhotic group were very similar to those that have been reported for primary hepatoma patients.
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PMID:Plasma and urine cyclic nucleotide levels in malignant disease and cirrhosis of the liver. 23 Feb 5

The atrial natriuretic peptide hormonal system is altered to a variable degree in patients with cirrhosis. Portal pressure and portal-systemic shunting are also varied in cirrhosis. We used a portal vein-ligated rat model with predictable portal hypertension to study the effects of portal hypertension alone on the atrial natriuretic peptide hormonal system. Sham-operated rats were used as controls. Mean portal pressure was significantly increased in portal vein-ligated rats (portal vein-ligated rats, 21.7 +/- 0.74 cm H2O; sham-operated rats, 13.7 +/- 0.47 cm H2O; p less than 0.0001). Plasma atrial natriuretic peptide decreased 50% in the portal vein-ligated rats (p less than 0.0001). Atrial natriuretic peptide messenger RNA level was decreased by 40% to 60% in the left and right atria and in the ventricles of portal vein-ligated rats (p less than 0.05 for each chamber). Only one class of glomerular binding site was identified by competitive binding studies. The atrial natriuretic peptide glomerular receptor density increased in the portal vein-ligated rats (portal vein-ligated rats, 1,660 +/- 393; sham-operated 725 +/- 147 fmol/mg protein, p less than 0.02), whereas affinity decreased (portal vein-ligated, 1.69 +/- 0.49; sham-operated, 0.55 +/- 0.12 nmol/L, p less than 0.02). No difference was seen in the amount of cyclic GMP generated by atrial natriuretic peptide stimulation in isolated glomeruli from portal vein-ligated and sham-operated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic peptide in portal vein-ligated rats: alterations in cardiac production, plasma level and glomerular receptor density and affinity. 131 88

Because it has been hypothesized that the hyperkinetic circulation in portal hypertension is the result of increased synthesis of nitric oxide, we compared the hemodynamic effects of nitric oxide synthesis--specific agonist (L-arginine) and antagonist between normal and cirrhotic conscious rats. The dose-response curves showed that L-arginine significantly decreased arterial pressure and increased heart rate. These changes started at the 200 mg/kg dose and were similar in both groups of rats. In both groups of rats NG-monomethyl-L-arginine (25 mg/kg) significantly decreased cardiac output by 35%. In cirrhotic rats, NG-monomethyl-L-arginine decreased portal pressure from 15.3 +/- 0.9 mm Hg to 13.6 +/- 0.7 mm Hg and portal tributary blood flow from 7.8 +/- 0.7 ml.min-1.100 gm-1 to 5.9 +/- 0.7 ml.min-1.100 gm-1; it significantly increased portal territory vascular resistance from 950 +/- 108 dyn.sec.cm-5.100 gm-1 x 10(3) to 1,579 +/- 258 dyn.sec.cm-5.100 gm-1 x 10(3). In normal rats, portal tributary blood flow decreased similarly, by 27%, and portal territory vascular resistance increased by 55%. In neither group was hepatic arterial blood flow altered. Before and after NG-monomethyl-L-arginine administration, arterial cyclic GMP concentrations were not significantly different between normal and cirrhotic rats. In conclusion, this study shows evidence of a normal role for nitric oxide-mediated vasodilatation in rats with cirrhosis and that inhibition of nitric oxide synthesis reduces portal hypertension. These results did not support the hypothesis that nitric oxide synthesis is increased in cirrhosis.
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PMID:Evidence for normal nitric oxide-mediated vasodilator tone in conscious rats with cirrhosis. 132 13

The effect of prostaglandins (PG) E1, E2, F2 and prostacyclin in vitro on the content of cAMP and cGMP in mononuclear cells of the blood was studied in 17 patients with liver cirrhosis. PG synthesis by mononuclears from 3H-arachydonic acid was also evaluated. Patients with liver cirrhosis showing no disorders of PG synthesis by non-stimulated mononuclears and reduction of basal cAMP content revealed significant changes of functional responses of cyclase systems PG loads as well as a relative reduction of PG synthesis in conditions of stimulation with phytohemagglutinin and Ca A23187 ionophore. This is an important link in deadaptation of immune reactions in patients with liver cirrhosis.
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PMID:[The role of prostaglandins in the activity of mononuclear cells in liver cirrhosis patients]. 148 97

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

We examined the acute effects of sinorphan, an inhibitor of enkephalinase, on plasma atrial natriuretic factor (ANF) and urinary sodium excretion in cirrhotic patients with ascites. A single oral dose of sinorphan (100 or 30 mg in 11 and 5 patients, respectively) was administered against placebo according to a double blind cross-over protocol. Basal plasma ANF levels varied over a large range between 2.6-79 pmol/L. Sinorphan, at a dose of 100 mg, inhibited 70% of plasma enkephalinase activity 60 min after ingestion and elicited simultaneously an increase in plasma ANF and cGMP levels 1.8 and 1.5 times basal values, respectively. There was a transient increase in sodium urinary output without a change in creatinine clearance over the initial 2-h period following drug administration. An increase in urinary cGMP was also observed on a longer period of 6 h. Plasma aldosterone decreased significantly, but the lowest concentration was reached 1 h later than the peak of plasma ANF. Mean blood pressure and PRA were unmodified. The effects of 30 mg sinorphan on plasma ANF, cGMP, and aldosterone were also significant, but less marked than those of the higher dose. Therefore, enkephalinase inhibition transiently increases sodium urinary excretion in cirrhotic patients with ascites via a mechanism that is likely to imply reduction of ANF catabolism. These results suggest that ANF could play a role in the control of sodium homeostasis in liver cirrhosis with ascites.
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PMID:Effect of sinorphan, an enkephalinase inhibitor, on plasma atrial natriuretic factor and sodium urinary excretion in cirrhotic patients with ascites. 184 6

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

Fifty three patients with liver cirrhosis and other chronic liver disease were divided into three different groups according to severity (group I: non-cirrhotic group, group II: compensated cirrhotic group, group III: decompensated cirrhotic group) and were studied with regard to their autonomic nervous and general nervous activity. To estimate the patients' autonomic nervous activity, they were examined on the following items: 1) their subjective symptoms, 2) orthostatic dysregulation, 3) coefficient of variation in R-R interval in ECG (CVR-R) at rest, 4) minimum heart rate (MHR) at night, CVR-R at MHR at night, disparity in MHR between day and night (all three of these items measured using the Holter ECG), 5) serum adrenalin, noradrenaline, cyclic AMP, and cyclic GMP. Meanwhile, general nervous activity was evaluated by measuring the reaction time to sound and light stimuli and by performing a number connection test. Cardiac function was also measured using radionuclide angiography to study its relationship to autonomic nervous disturbance in patients with chronic liver disease. The results of autonomic nervous function tests, especially CVR-R at rest, MHR at night, CVR-R at MHR at night and the disparity in MHR between day and night, indicated a marked lowering of autonomic nervous function in group III. In the serological examination, serum noradrenaline. and cyclic GMP levels were significantly higher in groups II and III. The evaluation of general nervous function showed that the reaction time to sound and light stimuli was significantly slower in group III than in group I. The cardiac function test revealed no statistically significant differences between the groups. In conclusion, autonomic nervous disturbance in patients with chronic liver disease seems to increase gradually as the disease progresses and to emerge as a distinct clinical symptom chiefly at the decompensated stage of liver cirrhosis.
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PMID:[Autonomic nervous activity in patients with chronic liver disease especially liver cirrhosis]. 201 37

The discovery of atrial natriuretic peptide (ANP) has modified our current understanding of the regulation of sodium metabolism. This peptide, of which the second messenger is cyclic guanosine monophosphate (cyclic GMP), is released by the atrial myocytes in response to increased atrial stretch and has for essential function to diminish the venous return to the heart. Radioimmunoassays have demonstrated that plasma ANP and cyclic GMP levels are increased in various diseases such as congestive heart failure (CHF), renal insufficiency, and, to a lesser extent, diabetes mellitus and liver cirrhosis with ascites. Plasma ANP is of prognostic value in CHF and reflects the effective central volemia in renal failure so that its assay as well as that of plasma cyclic GMP seem of interest in these diseases. Further studies are needed to assess the pathophysiological significance of ANP in diabetes mellitus and cirrhosis, and to define the indications of the treatment by enkephalinase inhibitors which increase endogenous ANP levels by lowering the catabolism of this hormone.
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PMID:Current indications of plasma atrial natriuretic peptide measurements in human diseases. 215 73


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