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)

Isoprenaline sensitivity and plasma catecholamine concentrations were studied to assess the sympathetic nervous activity in 13 patients with alcoholic cirrhosis and were compared with five controls. In patients with cirrhosis, the dose of isoprenaline required to increase the resting heart rate by 25 beats min-1 (chronotropic dose 25 or CD25) ranged from 2.50 to 34.73 micrograms (median: 4.47 micrograms) and was significantly higher than in controls (range: 0.66 to 2.76 micrograms, median: 1.34 micrograms). In cirrhotic patients, CD25 values were significantly correlated with plasma albumin concentration, resting heart rate and wedged hepatic venous pressure. In patients with cirrhosis, plasma noradrenaline concentrations ranged from 192 to 978 pg ml-1 (median: 444 pg ml-1) and adrenaline concentrations ranged from 5 to 183 pg ml-1 (median: 47 pg ml-1). No correlation was found between noradrenaline or adrenaline concentrations and CD25 values in cirrhotic patients. In conclusion, in patients with cirrhosis, beta-adrenoceptor responsiveness assessed by isoprenaline sensitivity is altered.
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PMID:Alterations in isoprenaline sensitivity in patients with cirrhosis: evidence of abnormality of the sympathetic nervous activity. 395 35

Plasma norepinephrine concentrations are elevated in patients with decompensated cirrhosis, and correlate inversely with urinary sodium and water excretion. Increased plasma norepinephrine concentrations may result from a decreased metabolic clearance rate or an increased secretion rate, possibly in response to a decreased "effective arterial blood volume." If the latter hypothesis is correct, plasma norepinephrine might be expected to be suppressed when central blood volume is expanded by head-out water immersion. In the present study, plasma norepinephrine secretion and clearance rates were determined by infusion of tritiated norepinephrine. Norepinephrine secretion rates were elevated in eight cirrhotic patients as compared to control subjects (1.50 +/- 0.25 vs. 0.26 +/- 0.08 micrograms/m2 per min, P less than 0.001), whereas clearance rates were similar (3.13 +/- 0.48 vs. 2.60 +/- 0.28 liters/min, NS). Baseline plasma norepinephrine concentrations were markedly elevated in the cirrhotic patients (830 +/- 136 vs. 185 +/- 12 pg/ml, P less than 0.001). Head-out water immersion significantly suppressed plasma concentrations of both norepinephrine (704 +/- 72 to 475 +/- 70 pg/ml, P less than 0.005) and epinephrine (121 +/- 33 to 57 +/- 10 pg/ml, P less than 0.05) in all seven patients studied. We conclude that the high circulating catecholamine concentrations in cirrhosis are secondary to increased secretion, rather than to decreased metabolic clearance, and are suppressible by central blood volume expansion.
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PMID:Elevated plasma norepinephrine concentrations in decompensated cirrhosis. Association with increased secretion rates, normal clearance rates, and suppressibility by central blood volume expansion. 397 17

Cardiovascular haemodynamics and circulating catecholamines were studied in 22 patients with cirrhosis. Arterial plasma noradrenaline (NA) was significantly increased (median, 0.48 ng/ml, versus controls, 0.24 ng/ml; n = 17; P less than 0.001), indicating enhanced sympathetic nervous activity. Heart rate was also increased (88 min-1 versus controls, 68 min-1; P less than 0.001), and mean arterial blood pressure was significantly decreased (81 mm Hg, versus controls, 88 mm Hg; P less than 0.002). Cardiac output was above the upper reference limit in eight patients and below the lower limit in two patients. Arterial NA was inversely correlated to stroke volume (r = -0.55; P less than 0.01) and to cardiac output (r = -0.53; P less than 0.02). Statistically significant relationships could not be demonstrated between NA and heart rate, arterial blood pressure, or right atrial pressure, but NA was slightly positively correlated to systemic vascular resistance (r = 0.51; P less than 0.02). The results may suggest that a relatively insufficient cardiac performance in the hyperkinetic circulatory state in cirrhosis may elicit an enhanced sympathetic nervous activity, which may contribute to maintenance of cardiovascular homeostasis.
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PMID:Circulating noradrenaline and central haemodynamics in patients with cirrhosis. 409 92

In 20 patients with g hepatic cirrhosis hospitalized for upper digestive haemorrhage by rupture of oesophageal varices, the intragastric administration of norartrinal in amounts of 4-40 mg/24 h achieved definitive haemostasis in 7 cases and temporary haemostasis (with prolonged survival) in another 6 cases. The overall mortality was 80%. In three of the 7 patients in which haemorrhage was completely arrested death occurred as a result of hepatic failure. The large amounts of Norartrinal administered (up to 120 mg total dose) were well tolerated and did not have haemodynamic side-effects, or renal side-effects. The results obtained, and especially the easy method used for administration of the drug recommend this method as an alternative of the vasopressin treatment.
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PMID:[Intragastric administration of norartrinal in hemorrhage caused by rupture of esophageal varices]. 621 26

Plasma noradrenaline (NA) and adrenaline (A) concentrations were determined in different vascular areas in 32 patients with cirrhosis and in nine controls during a right sided heart, liver, and renal vein catheterisation. The patients were divided into four groups: (I) Compensated (without ascites); (II) Recompensated on diuretic treatment because of former ascites; (III) Decompensated (with ascites) without treatment and (IV) Decompensated on diuretic treatment. Median arterial noradrenaline concentrations were 1.48, 1.07, 2.66, 4.14 and 2.50 nmol/l in controls, group I, II, III, and IV, respectively, the three last mentioned values being significantly raised (p less than 0.01). Median arterial adrenaline concentrations were not significantly increased. In patients arterial-hepatic venous extraction ratios of noradrenaline and adrenaline were on the average 25% (p less than 0.01) and 20% (p less than 0.02) less than those of the controls, indicating a slightly reduced splanchnic elimination of catecholamines in cirrhoses. In controls and group I significant renal venous-arterial noradrenaline differences were absent (0.00 and 0.03 nmol/l) while renal venous-arterial noradrenaline differences were significantly increased in groups II, III and IV (0.47, 0.53 and 0.68 nmol/l, p less than 0.01), indicating a significant net release of noradrenaline from the kidneys in recompensated and decompensated patients. Renal extraction of adrenaline was normal. In conclusion, increased arterial noradrenaline in decompensated and recompensated cirrhosis is only to a limited extent owing to reduced net splanchnic elimination. More likely the increase is caused by release of noradrenaline from the kidneys and possibly other organs indicating enhanced sympathetic nervous tone in these conditions.
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PMID:Splanchnic and renal elimination and release of catecholamines in cirrhosis. Evidence of enhanced sympathetic nervous activity in patients with decompensated cirrhosis. 647 78

The purpose of this study was to determine if the renal circulation of normal and cirrhotic dogs behave similarly in response to an acute endotoxin infusion. Endotoxin was administered as a slow continuous infusion (13-26 micrograms/min) to a total of 20 normal dogs through the femoral vein, portal vein, or into the left renal artery. In each case, there was an initial increment in renal blood flow, of the order of 46%, while arterial blood pressure was actually declining. After 8-20 min, blood flow fell as perfusion pressure declined further. The initial increment in renal perfusion was not due to a hyperthermic response following the endotoxin. When similar doses were given to five dogs with chronic biliary cirrhosis and ascites, the biphasic response in renal perfusion was not observed, rather blood flow declined as perfusion pressure declined. When normal dogs were infused with bilirubin, bile salts, noradrenaline, and angiotensin in pressor doses, the subsequent infusion of endotoxin still produced the usual biphasic response in renal perfusion. Chronic elevation of portal pressure (but not acute elevation), volume contraction by diuresis or hemorrhage, and the infusion of bile intravenously, all abolished the biphasic response in renal perfusion and reproduced in normal dogs the response to endotoxin observed in cirrhotic dogs. Investigation of the factors causing the initial decrease in intrarenal vascular resistance in normal dogs following the endotoxin infusion implicated a role for histamine, kinins, and prostaglandins. We conclude there is a fundamental difference in the response of the renal circulation of normal and cirrhotic dogs to an endotoxin infusion, which may depend on failure of this latter group to release one or more humoral agents. This difference may be due to elevated portal pressure, a decreased effective arterial blood volume, or the products of bile having access to the circulation in cirrhotic dogs.
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PMID:Renal blood flow in normal dogs and in dogs with experimental liver cirrhosis following the acute continuous infusion of endotoxin. 666 92

Splanchnic extraction rates of adrenaline and noradrenaline were determined in seven normal subjects and in nine patients with cirrhosis of the liver using arterial-hepatic venous catherization . Both catecholamines were effectively removed when the blood passed through the splanchnic area: splanchnic fractional uptake of adrenaline in normal subjects was 90 +/- 3%, and lower for noradrenaline, 68 +/- 4% (P less than 0.001). Net splanchnic extraction rates were higher for noradrenaline (126 +/- 16 ng/min) than for adrenaline (40 +/- 10 ng/min, P less than 0.001), probably due to the higher arterial plasma levels of noradrenaline. Resting arterial adrenaline and noradrenaline levels were significantly higher in cirrhotic patients than in normal subjects (adrenaline: 121 +/- 27 vs 54 +/- 8 pg/ml, P less than 0.05; noradrenaline: 678 +/- 89 vs 251 +/- 26 pg/ml, P less than 0.005). Net splanchnic catecholamine uptake was increased in cirrhotic patients. The results demonstrate that the splanchnic bed in normal and cirrhotic subjects extracts plasma catecholamines efficiently; they suggest that elevated plasma catecholamines in cirrhosis are not the result of impaired splanchnic catecholamine removal.
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PMID:Role of the splanchnic bed in extracting circulating adrenaline and noradrenaline in normal subjects and in patients with cirrhosis of the liver. 673 77

Hepatic encephalopathy (HE) is currently felt to be secondary to a disturbance in the metabolism of cerebral catecholamines with a decline in dopamine and noradrenaline and a rise in the false neurotransmitter octopamine. The aim of this study was to evaluate brain tissue levels of dopamine, noradrenaline, and octopamine in patients with cirrhosis and HE. This study includes 34 patients: 22 were cirrhotic, 12 were control subjects. Among the 22 cirrhotic patients, 19 had HE, three did not. Tissue specimens were obtained at necropsy from the locus niger, caudate nucleus, hypothalamus, thalamus and frontal cortex, and from the frontal cortex during neurosurgical procedures. Our results showed that (1) dopamine and noradrenaline levels are identical in cirrhotic patients with or without HE and in patients without liver disease (P < 0.05); (2) octopamine levels are higher in control subjects than in patients with cirrhosis and HE. In conclusion, there is no decline in dopamine and noradrenaline levels in the brain tissues of cirrhotic patients with HE, and this is in contradication with the animal findings; octopamine levels are not raised. Hepatic encephalopathy in human liver cirrhosis does not seem to be secondary to a disturbance in cerebral catecholamines.
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PMID:Changes in brain catecholamine levels in human cirrhotic hepatic encephalopathy. 677 15

1. The metabolic effect of alpha-oxoisocaproate (4-methyl-2-oxovalerate) infusion was examined in six patients with cirrhosis and in nine healthy control subjects. The arterial concentrations of amino acids, urea, ammonia, insulin and catecholamines were determined in the basal state and during intravenous infusion of alpha-oxoisocaproate (300 mumol/min) for 150 min. The exchanges of amino acids and substrates across the splanchnic region, the brain and the leg were examined in the healthy subjects by a catheter technique. 2. Basal alpha-oxoisocaproate levels were similar in patients and control subjects. During infusion the concentrations of alpha-oxoisocaproate rose to 90-130 mumol/l; they were 20-35% lower in the patients. Arterial leucine concentration increased in both groups to 250-300 mumol/l. Valine and isoleucine concentraions decreased (50-60%) as did to a lesser extent the concentrations of aromatic amino acids and methionine. 3. Regional exchange of amino acids was not significantly influenced by alpha-oxoisocaproate infusion. Arterial urea concentration decreased (12%, P less than 0.05) and ammonia levels rose (15-25%, P less than 0.05) in both groups. In the patients both adrenaline (100%, P less than 0.001) and noradrenaline concentrations were elevated (350%, P less than 0.001) in the basal state; insulin levels were similar to those in control subjects. 4. It is concluded that alpha-oxoisocaproate is rapidly transaminated to leucine in patients with cirrhosis and in healthy control subjects. alpha-Oxoisocaproate infusion resembles leucine infusion in its influence on aromatic amino acid concentrations, but in addition it elicits increased ammonia levels and decreased urea formation.
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PMID:Intravenous infusion of alpha-oxoisocaproate: influence on amino acid and nitrogen metabolism in patients with liver cirrhosis. 706 Mar 35

Plasma noradrenaline (NA) and adrenaline (A) concentrations were related to various haemodynamic parameters in fifteen patients with cirrhosis. In supine position at rest plasma NA and A in peripheral venous blood were significantly higher in patients with cirrhosis than in normal subjects. Mean plasma NA averaged 0.66 and 0.21 ng/ml, respectively (P less than 0.01). The corresponding values for plasma A were 0.14 and 0.05 ng/ml (P less than 0.03). Splanchnic arterial-hepatic venous extraction ratio of NA in patients with cirrhosis averaged 0.46 (P less than 0.01). The right kidney released NA into the systemic circulation. Renal venous plasma NA exceeded arterial concentration by 38% (P less than 0.02). NA concentrations in femoral vein and ascitic fluid were not different from that of arterial plasma. Plasma NA was positively correlated to wedged hepatic vein pressure (r = 0.86, P less than 0.001) and to heart rate (r = 0.61, P less than 0.02), but inversely correlated to plasma volume (r = 0.83, P less than 0.01) in cirrhotic patients. Arterial blood pressure was reduced in these patients compared to controls (P less than 0.02), but not significantly correlated to plasma NA. The increased plasma NA indicates that sympathetic nervous activity is enhanced in patients with cirrhosis. Based on the above positive correlation between NA and heart rate and the significant release of NA from the kidney, it may be hypothesized that the increased sympathetic nervous activity especially involves heart and kidney. This response may be mediated by baro- and volume receptors.
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PMID:Noradrenaline and adrenaline concentrations in various vascular beds in patients with cirrhosis. Relation to haemodynamics. 719 89


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