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Platelet uptake of octopamine and norepinephrine in hepatic encephalopathy



Platelet uptake of octopamine and norepinephrine in hepatic encephalopathy



Gastroenterology 73(3): 560-564



To explore platelets as a model of intracellular [neuronal] amine metabolism in liver disease, platelet uptake of octopamine (OA) was studied in controls and patients with hepatic encephalopathy (HE), and the influence of OA and plasma from patients with HE on platelet norepinephrine uptake was investigated. Normal platelets incubated at 37.degree. C actively accumulated OA. A high ratio of platelet OA concentration to plasma concentration (30:1) and inhibition of platelet OA uptake at reduced temperature suggested uptake by an active process. More than 90% of AO accumulated by platelets was recovered intact after 1 h. Thrombin released 40% of platelet OA, suggesting sequestration within amine storage granules. OA inhibited the uptake of [3H] norepinephrine (NE) by platelets, suggesting that these substances share the same transfer system. Platelets of patients with HE demonstrated decreased uptake of OA and NE. Inhibition of platelet OA uptake was proportional to the clinical stage of HE. Plasma from patients with HE inhibited NE uptake by normal platelets. Plasma OA and/or other amines are apparently taken up by platelets where they are protected from degradation. The reduced uptake of OA and NE by platelets from patients with HE could result from uptake blockade by intraplatelet amines and/or inhibition of platelet amine uptake by plasma amines. The demonstration of altered platelet OA and NE metabolism in patients with encephalopathy suggested that this model may be useful for the study of intracellular amines in liver disease.

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Accession: 006135217

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PMID: 330303



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