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octopamine/fibrose
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15 Ergebnisse
The cardiorespiratory impairment in cirrhosis and sepsis. An experimental interpretation using octopamine infusion.
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The effects of octopamine on systemic and pulmonary circulation and on respiratory parameters have been studied in ten O2 100% breathing pigs. A rise in cardiac index (CI) due to an increase in the dynamics of the left ventricle and a progressive hypoxemia, notwithstanding the hyperventilation, was
Plasma catecholamines in hepatic coma and liver cirrhosis: role of octopamine.
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Pathogenesis of hepatic encephalopathy and hyperdynamic syndrome in cirrhosis. Role of false neurotransmitters.
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We sought to determine whether false neurotransmitters (FNTs) play an important role as determinants not only of hepatic encephalopathy but also of hyperdynamic syndrome in cirrhosis. A combined biochemical and hemodynamics study of 55 bleeding cirrhotic patients was made. We evaluated the aromatic
The altered plasma amino acid pattern is responsible for the paradoxical growth hormone response to the oral glucose tolerance test in liver cirrhosis.
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OBJECTIVE
An increased basal growth hormone (GH) secretion and a parodoxical GH response to the oral glucose tolerance test (OGTT) have been reported in patients with liver cirrhosis. It has been suggested that the ratio between branched-chain amino acids (BCAAs) and aromatic amino acids (AAAs)
Effects of octopamine on renal function in anaesthetized dogs.
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Increased levels of octopamine in adrenergic nerve terminals and plasma have been implicated in the circulatory and renal disturbances of chronic hepatic failure. Little is known about its renal actions in normal animals. In the present study, DL-octopamine was administered both i.v. and into one
Deranged tyrosine metabolism in cirrhosis.
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In normal individuals, the main route for tyrosine degradation is the hepatic pathway tyrosine→4-hydroxyphenylpyruvic acid→homogentisic acid→CO(2). Quantitatively minor pathways, in large part extrahepatic, are: tyrosine→tyramine→octopamine and tyrosine→dopa→catecholamines.In cirrhosis, the main
Pathologic synergy in cardiovascular and respiratory compensation with cirrhosis and sepsis. A manifestation of a common metabolic defect?
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Multivariable physiologic studies of cardiovascular, respiratory, and metabolic functions were performed in 341 patients (884 studies). Eighty patients had cirrhotic liver disease, 64 had sepsis, 87 had nonseptic cariogenic syndromes, and 110 had nonseptic general surgical or traumatic injury. The
Vasoactive factors in decompensated cirrhosis. Effect of acute plasma expansion.
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Plasma volume expansion was performed in 16 cirrhotic patients with ascites, 8 with avid sodium retention (sodium retainers) and 8 with normal sodium balance (sodium excretors). No natriuretic response was observed in sodium retainers (daily UNa = 7.1 +/- 1.5 mEq before expansion and 20.8 +/- 7.8
Plasma phenylethanolamine in hepatic encephalopathy.
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It has been suggested that amines other than octopamine may be involved in the pathogenesis of hepatic encephalopathy. Plasma phenylethanolamine has been determined by a radioenzymatic method in twenty-six biopsy-proven cirrhotics with or without encephalopathy and in seven normal adults.
Visual evoked potential: a diagnostic tool for the assessment of hepatic encephalopathy.
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Visual evoked potential recordings were examined in 45 liver cirrhosis patients with (n = 29) and without (n = 16) encephalopathy, in 15 normal volunteers, and in one patient with an opioid induced stupor state. Visual evoked potential parameters were classified on the basis of EEG recordings.
Vasoactive factors in the mechanism of renal sodium handling in cirrhotics: the effect of acute plasma expansion.
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Twenty cirrhotic patients with ascites, divided into two groups of 10 each, according to their daily urinary sodium excretion (sodium retainers and sodium excretors) and given a diet of 75 mEq of sodium daily, underwent acute plasma volume expansion with 1,000 ml of 10% dextran in saline, infused
[Hepatic encephalopathy. Pathogenesis and therapy].
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Hepatic encephalopathy is a frequent complication of cirrhosis. Portal-systemic shunts and depression of hepatic function are the primary underlying abnormalities. Arterial blood ammonia levels are frequently elevated during hepatic encephalopathy and are lower when a clinical improvement is
[Pathogenesis of hepatic encephalopathy (author's transl)].
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This contribution presents data from the literature as well as our own results concerning the mechanisms of hepatic encephalopathy (HE). 1. Blood chemistry: In patients with liver cirrhosis, the plasma levels of ammonia, phenylalanine, tyrosine, phenolic acids, and octopamine correlated with the
Dopamine uptake by platelets in hepatic encephalopathy; evidence for a possible depletion of brain dopamine.
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A decrease in H3-dopamine uptake was demonstrated in the blood platelets of 22 hepatic encephalopathy (HE) patients when compared to that of patients with liver cirrhosis, but without HE, and controls. There was a direct correlation between the stage of HE and the decrease in H3-dopamine uptake. As
Changes in brain catecholamine levels in human cirrhotic hepatic encephalopathy.
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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,
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