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Effects of propofol on desipramine-sensitive [3H]-noradrenaline uptake kinetics in rat femoral artery

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Background:

The intravenous anaesthetic propofol inhibits the neuronal uptake of noradrenaline (uptake1) from the vascular sympathetic neuromuscular junction, resulting in an enhancement of the sympathetic neurotransmission. This could be important for maintenance of blood pressure during propofol anaesthesia. The aim of the present study was to determine how propofol influences the kinetics of uptake1. Methods:

Isolated segments of rat femoral arteries were incubated with [3H]-noradrenaline in the presence or absence of propofol and the radioactivity taken up was measured in a scintillation counter. The uptake1 inhibitor, desipramine, was used to delineate the specific neuronal uptake. Results:

Desipramine and 10 μM propofol significantly reduced the uptake in segments incubated with 0.1 μM [3H]-noradrenaline. Propofol at 1 μM and 100 μM did not affect the uptake. Non-linear regression analysis of specific uptake yielded Km 0.50 μM, Vmax 1.6 pmol mg−1 15 min−1 and Hill coefficient 1.1. Propofol (1–10 μM) increased the Km value and propofol (10–100 μM) increased the Vmax value concentration-dependently, while the Hill coefficient was not affected. Conclusion:

Propofol seems to have a biphasic effect on the uptake of noradrenaline in the vascular sympathetic neuromuscular junction. At lower propofol concentrations there is a decrease in the affinity of the noradrenaline transporters. The resulting uptake inhibition is counteracted at higher propofol concentrations by an increase in the efficacy of the uptake.
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Keywords: Propofol; femoral artery; kinetics; noradrenaline; rats; sympathetic nervous system; uptake

Document Type: Research Article

Affiliations: 1: Department of Anaesthesia and Intensive Care, University Hospital, Lund, and 2: Department of Anaesthesia and Intensive Care, Hospital of Helsingborg, Helsingborg, Sweden

Publication date: 2000-09-01

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