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  • 1
    ISSN: 1432-1440
    Keywords: Catecholamines ; Octopamine ; Hepatic coma ; Sympathetic nervous system ; Katecholamine ; Octopamin ; Coma hepaticum ; Sympathisches Nervensystem
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Plasmaspiegel von Adrenalin, Noradrenalin und Octopamin wurden mit Hilfe radioenzymatischer Methoden bei neun ambulanten Zirrhose-Patienten mit Enzephalopathie und bei zehn Patienten im Coma hepaticum (Comagrad III–IV) bestimmt. Bei den Zirrhose-Patienten wurden sowohl normale als auch erhöhte Plasmaspiegel von Noradrenalin gemessen. Octopamin war im Plasma dieser Patienten sowie bei zehn gesunden Kontrollpersonen nicht nachweisbar. Erhöhte Noradrenalinspiegel im Plasma waren bei allen Patienten im Coma hepaticum vorhanden. Die Noradrenalinkonzentration im Plasma blieb auch während des Comaverlaufes erhöht oder stieg weiter an. Der Adrenalinplasmaspiegel war hingegen nicht regelmäßig erhöht. In acht der zehn Patienten war Octopamin wiederum nicht nachweisbar. Nur bei zwei Coma-Patienten konnten Octopaminspiegel bis zu 59,5 ng/ml bei gleichzeitiger Erhöhung der Noradrenalinkonzentration gefunden werden. Die Infusion der verzweigtkettigen Aminosäure L-Valin beeinflußte weder den Noradrenalin- noch den Octopaminspiegel. Die Ergebnisse sprechen dafür, daß die Aktivität des sympathischen Nervensystems im Coma hepaticum erhöht ist. Eine Akkumulierung von Octopamin ist kein charakteristischer Befund bei chronischer Lebererkrankung und hepatischem Coma. Nachdem bei zwei Coma-Patienten die Akkumulierung von Octopamin bei einer gleichzeitigen Erhöhung des Noradrenalinspiegels auftrat, erscheint eine Verdrängung von Noradrenalin durch den falschen Neurotransmitter Octopamin im noradrenergen Neuron des peripheren Sympathikus unwahrscheinlich. Die Resultate sprechen dafür, daß die Entwicklung einer Hypotension im Rahmen der Leberzirrhose und des Coma hepaticum nicht auf einen Mangel an Noradrenalin zurückzuführen ist.
    Notes: Summary Plasma levels of adrenaline, noradrenaline and octopamine were estimated by a radioenzymatic method in nine cirrhotic outpatients with encephalopathy and in ten patients with hepatic coma (coma grade III–IV). In the cirrhotic outpatients normal as well as elevated plasma levels of noradrenaline were found. Octopamine could not be detected in the plasma of these patients as well as of ten healthy volunteers. Elevated noradrenaline levels were present in all patients with hepatic coma. Plasma noradrenaline remained elevated or even further increased during the course of hepatic coma, whereas adrenaline was elevated less frequently. In eight of the ten patients with hepatic coma octopamine was again not detectable in plasma. Only in two patients high levels of octopamine up to 59.5 ng/ml could be found in addition to increased noradrenaline concentrations. The infusion of the branched chain amino acid L-valine had no influence on the plasma level of either noradrenaline or octopamine. The data indicate that the sympathetic nervous system is activated during the course of hepatic coma. An accumulation of octopamine is not a common finding in chronic liver disease and hepatic coma. Since in the two patients with elevated octopamine levels the rise in octopamine occured concomitantly with a rise in noradrenaline, a displacement of noradrenaline by the false neurotransmitter octopamine in the noradrenergic neuron of the peripheral sympathetic nervous system seems unlikely. The results indicate that the development of hypotension in the course of liver cirrhosis and hepatic coma cannot be related to a deficiency of noradrenaline.
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  • 2
    ISSN: 1432-1238
    Keywords: Severe cerebral trauma ; Midbrain syndrome ; Apallic syndrome ; Catecholamines ; Fat oxidation ; Thyroid hormones ; High caloric total parenteral alimentation (TPA)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Urinary catecholamine excretion and thyroid hormone blood level were studied in 16 patients following severe cerebral trauma. Increased excretion rates of epinephrine and norepinephrine were found. There was no significant difference in the catecholamine excretion when compared with generally traumatized patients. The relationships between catecholamine excretion, increased metabolic rates, and negative nitrogen balance indicate that in patients with a midbrain syndrome there exists an additional diencephalic metabolic factor, which leads to a rise in fat oxidation and perpetuation of catabolism. Early high caloric parenteral nutrition seems to inhibit the initial increase of catecholamine excretion and thus protects the body from an unnecessary breakdown of its own reserves. If the course is classified according to neurological stages, it can be shown that patients with a traumatic apallic syndrome in poor condition have a high increase of catecholamine excretion. Secretion of thyroid hormones is not influenced significantly by cerebral trauma.
    Type of Medium: Electronic Resource
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