Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

One hundred and eight patients with cirrhosis (23 grade A, 46 grade B and 39 grade C, according to Pugh's classification) underwent hemodynamic studies and plasma catecholamine concentration measurements. Blood samples were withdrawn from the pulmonary artery (n = 108), the hepatic vein (n = 108), the azygos vein (n = 59), the right renal vein (n = 66), the right jugular vein (n = 34) and the femoral vein (n = 33). Plasma noradrenaline concentrations in the pulmonary artery and the hepatic vein were more elevated in grade B (607 +/- 52 and 402 +/- 42 pg/ml, respectively) and C patients (630 +/- 59 and 475 +/- 53 pg/ml, respectively) than in grade A patients (411 +/- 51 and 243 +/- 40 pg/ml, respectively). Plasma noradrenaline concentrations from these two vessels were negatively correlated with indocyanine green clearance. These results indicate that both overall and splanchnic sympathetic activities are dependent on altered hepatic function. Significant correlations were found between the wedged hepatic venous pressure and plasma noradrenaline concentrations from either the pulmonary artery, the hepatic vein or the azygos vein. These correlations indicate that both overall and splanchnic sympathetic activities are dependent on the degree of portal hypertension. Moreover, significant correlations were found between hepatic venous plasma noradrenaline concentrations and systemic hemodynamic values, suggesting that splanchnic sympathetic nervous activity could either play a role in the systemic hyperkinetic syndrome or be a consequence of this hyperkinetic syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional sympathetic activity, severity of liver disease and hemodynamics in patients with cirrhosis. 174 20

In 11 patients with decompensated cirrhosis and deteriorating renal function, the effect of the vasoconstrictor substance 8-ornithin vasopressin (ornipressin; POR 8; Sandoz, Basel, Switzerland) on renal function, hemodynamic parameters, and humoral mediators was studied. Ornipressin was infused at a dose of 6 IU/h over a period of 4 hours. During ornipressin infusion an improvement of renal function was achieved as indicated by significant increases in inulin clearance (+65%), paraaminohippuric acid clearance (+49%), urine volume (+45%), sodium excretion (+259%), and fractional elimination of sodium (+130%). The hyperdynamic circulation was reversed to a nearly normal circulatory state. The increase in systemic vascular resistance (+60%) coincided with a decrease of a previously elevated renal vascular resistance (-27%) and increase in renal blood flow (+44%). The renal fraction of the cardiac output increased from 2.3% to 4.7% (P less than 0.05). A decline of the elevated plasma levels of noradrenaline (2.08-1.13 ng/mL; P less than 0.01) and renin activity (27.6-14.2 ng.mL-1.h-1; P less than 0.01) was achieved. The plasma concentration of the atrial natriuretic factor increased in most of the patients, but slightly decreased in 3 patients. The decrease of renal vascular resistance and the increase of renal blood flow and of the renal fraction of cardiac output play a key role in the beneficial effect of ornipressin on renal failure. These changes develop by an increase in mean arterial pressure, the reduction of the sympathetic activity, and probably of an extenuation of the splanchnic vasodilation. A significant contribution of atrial natriuretic factor is less likely. The present findings implicate that treatment with ornipressin represents an alternative approach to the management of functional renal failure in advanced liver cirrhosis.
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PMID:Ornipressin in the treatment of functional renal failure in decompensated liver cirrhosis. Effects on renal hemodynamics and atrial natriuretic factor. 183 7

The kinetics of plasma noradrenaline (NA) were studied in 14 patients with cirrhosis and ascites and 13 normal subjects. [3H]noradrenaline ([3H] NA) was infused intravenously to steady state and the spillover of NA into plasma and its clearance from plasma calculated. The increase in plasma NA in the cirrhotic patients was due to an increase in NA spillover (14.5 vs 3.9 nmol min-1m-2; P less than 0.001). NA plasma clearance was also increased in the cirrhotic patients (3.5 vs 2.11 min-1m-2; P less than 0.01). Plasma NA and dihydroxyphenylglycol (DHPG), a metabolite of NA of which a portion is formed after re-uptake of NA into sympathetic nerve endings, were then measured in 23 patients with cirrhosis and ascites, 17 patients with cirrhosis who had never had ascites, and 34 normal subjects. Both plasma NA and DHPG were significantly increased in the patients with ascites (NA 4.7, DHPG 14.7 nmol l-1 and in the patients with cirrhosis but no ascites (NA 3.8, DHPG 12.0 nmol l-1) compared with normal subjects (NA 1.9, DHPG 8.8 nmol 1-1). Therefore, the increase in plasma NA in cirrhosis is due to increased activity of the sympathetic nervous system rather than interference with the metabolism of NA or impaired neuronal uptake of NA. This increase appears to precede the development of ascites.
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PMID:Plasma noradrenaline in cirrhosis: a study of kinetics and temporal relationship to ascites formation. 190 38

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

Patients with cirrhosis, especially those with decompensated disease have enhanced sympathetic nervous activity. We have investigated the effect of a single oral dose of 80 mg propranolol on circulating catecholamines and related the effect to splanchnic and systemic haemodynamics in 22 patients with cirrhosis. Plasma noradrenaline (NA) was significantly above normal average (NA: 0.52 vs. 0.23 ng/ml, p less than 0.01) and increased with the severity of the liver disease (p less than 0.01). NA was negatively correlated with liver function as estimated by ICG clearance (r = -0.74, p less than 0.01). Azygos blood flow was increased (0.75 l/min) and positively related to plasma NA (r = 0.57, p = 0.05, n = 12). After propranolol intake, plasma NA increased from 0.52 to 0.59 ng/ml (p less than 0.01). This response was found in all Child-Turcotte classes (A: 0.37 to 0.43; B: 0.49 to 0.56; C: 0.78 to 0.88 ng/ml), and in patients with as well as without ascites. Plasma adrenaline increased in the same way (p less than 0.01). Hepatic blood flow (from 1.10 to 0.93 l/min, p less than 0.01) and azygos blood flow (from 0.75 to 0.55 l/min, n = 9, p less than 0.05) decreased significantly after oral propranolol. A borderline significant correlation was observed between the decrease in azygos blood flow and the increase in NA (r = 0.64, p = 0.06). Our results suggest that besides a relationship to liver function and severity of disease, sympathetic nervous activity, as reflected by circulating NA, will further enhance during beta-adrenergic blockade, probably by a compensatory mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of oral propranolol on circulating catecholamines in cirrhosis: relationship to severity of liver disease and splanchnic haemodynamics. 233 91

The noradrenaline (NA) that has diffused from sympathetic synapses into plasma can be assayed accurately and reliably in plasma, as it is the best index of sympathetic activity. A considerable advance has been achieved by using infusions of tritium-labelled exogenous NA, such infusions being devoid of functional effect. By measuring simultaneously blood NA levels and circulating tritiated NA levels the amplitude of synaptic spillover and therefore of sympathetic activity can be evaluated and the metabolic NA clearance can be measured. Synaptic NA spillover and NA metabolic clearance were measured in 24 physiological, pathological and pharmacological situations, providing an accurate definition of the sympathetic states explored. By combining these techniques with selective vascular catheterization, the sympathetic activity of the organs explored can be assessed, and regional sympathetic activities are currently being mapped. Such regional studies are of great value to understand the mechanisms involved in heart failure, cirrhosis or arterial hypertension. Sympathetic system regulations result from a central influence and from peripheral adjustments that are potentially specific to each organ.
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PMID:[Plasma noradrenaline. Significance and practical value of its determination]. 253 59

The aim of this study is at establishing cirrhotic portal hypertension with common bile duct ligation in 9 mongrel dogs to measure the plasma catecholamine level. On the basis of experimental study, phentolamine, the alpha-adrenoceptor antagonist, was used to treat 14 patients with liver cirrhosis complicating bleeding from esophageal variceal rupture. The results had been shown that the levels of noradrenaline (NE) in both portal and inferior caval vein were increased more significantly in the cirrhotic stage than in the precirrhotic stage. The mechanism of the NE elevation might be due to increased release from enhancement of sympathetic nervous activity. Our clinical data have also been demonstrated that the effect of phentolamine on the 12 cases of variceal hemorrhage is markedly efficacious with no longer bleeding. Only 2 patients had showed no good reaction neither to phentolamine nor to pituiterin, eventually died of liver failure. It is conceivable that phentolamine has the same efficacy in treatment of esophageal variceal bleeding as pituitrin. But less side effect than the latter.
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PMID:[Phentolamine in cases of liver cirrhosis with bleeding from esophageal variceal rupture]. 262 24

Plasma noradrenaline and adrenaline concentrations were measured in 75 patients with cirrhosis in order to attempt to correlate these concentrations and liver failure and hemodynamic changes. The increased noradrenaline concentration was not correlated with the degree of liver failure estimated by Pugh's classification, with the cause of cirrhosis, with the presence of acute alcoholic hepatitis or with the presence of ascites. Adrenaline concentration was higher in cirrhotic patients with acute alcoholic hepatitis than in those without these lesions. Noradrenaline concentration was significantly correlated with heart rate, wedged hepatic venous pressure and renal blood flow. Noradrenaline concentration was also negatively correlated with stroke volume and adrenaline concentration was negatively correlated with cardiac output and stroke volume. These findings confirm the relationships between portal hypertension, sympathetic hyperactivity and renal function in patients with cirrhosis.
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PMID:[Relation between plasma catecholamines, the severity of the liver disease and hemodynamics in patients with cirrhosis]. 268 Jul 27

We measured the plasma concentration of a centrally derived noradrenaline (NA) metabolite, 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG), in 20 cirrhotic patients (eight with (group A) and 12 without (group B) hepatic encephalopathy (HE] and in 14 age matched healthy subjects to study if the central NA metabolism would be altered in liver cirrhosis patients, particularly in those with HE. The mean (SEM) plasma MHPG concentrations in the patient groups, group A (74.9 (8.6) pmol/l) and B (54.8 (7.2) pmol/l), were significantly (p less than 0.01) greater than in the control group (22.3 (2.0) pmol/l), and that in group A was significantly (p less than 0.05) greater than in group B. The plasma concentration of MHPG observed in these study subjects (n = 34) correlated (rs = 0.77, p less than 0.01) more strongly with the ratio of plasma catecholamine precursor amino acids (tyrosine and phenylalanine) to other neutral amino acids (tryptophan, leucine, isoleucine, and valine) known to compete with catecholamine precursor amino acids for uptake into the brain than with plasma concentration of tyrosine plus phenylalanine alone (rs = 0.63, p less than 0.01). In addition, the mean plasma MHPG concentrations measured in another group of eight cirrhotic patients (group C) during HE (79.3 (10.6) pmol/l) was significantly (p less than 0.01) greater than that measured after the recovery from HE (47.2 (5.2) pmol/l). The results suggest that the central NA metabolism may be altered in patients with liver cirrhosis, particularly in those with HE, and that the derangement in the central NA metabolism may be associated not only with an increase in plasma catecholamine precursor amino acids but also with a decrease in branched chain amino acids.
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PMID:Raised plasma concentrations of 3-methoxy-4-hydroxyphenylethyleneglycol in cirrhotic patients with or without hepatic encephalopathy. 273 59

The effects of clonidine on portal pressure and splanchnic blood flow were studied in conscious rats with sinusoidal portal hypertension due to cirrhosis induced by bile duct ligation. In cirrhotic and sham-operated rats, clonidine (20 micrograms per kg body weight, intravenously) significantly reduced portal, pressure from 19.0 +/- 0.6 to 14.5 +/- 1.0 mmHg and from 9.8 +/- 0.9 to 7.3 +/- 0.5 mmHg, respectively. No significant change in systemic hemodynamics was observed. In cirrhotic rats, clonidine reduced portal pressure, probably by producing a significant increase in portal tributary vascular resistance leading to a 25% decrease in portal tributary blood flow (radioactive microsphere method). In sham-operated rats, clonidine reduced portal pressure presumably by decreasing hepatic portal vascular resistance, since no significant change in portal tributary blood flow was observed. In both groups, clonidine administration significantly decreased plasma noradrenaline concentration. Placebo administration produced neither significant hemodynamic nor significant plasma noradrenaline concentration change. These findings indicate that the sympathetic regulation of the splanchnic circulation is impaired in cirrhotic rats.
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PMID:Mechanisms of a clonidine-induced decrease in portal pressure in normal and cirrhotic conscious rats. 277 9


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