Anaesthetics and the blood vessel wall. Actions of propofol and sevoflurane on sympathetic and endothelial control of smooth muscle function

Detta är en avhandling från Department of Anaesthesiology and Intensive Care, Lund

Sammanfattning: The anaesthetics we use today dose-dependently decrease the mean arterial pressure partly due to direct or indirect effects on the blood vessels. In the present thesis human omental arteries and veins and rat femoral arteries were investigated in vitro concerning the effects of the intravenous anaesthetic propofol and the volatile anaesthetic sevoflurane on the function of the perivascular sympathetic nerves and the endothelial cells. The effects of propofol on the kinetics of the neuronal uptake of noradrenaline were studied in the rat femoral artery. At lower propofol concentrations we found a decrease in the affinity of the noradrenaline transporters, which results in an uptake inhibition. At higher propofol concentrations this inhibition is counteracted by an increase in the efficiency of the uptake. The effects of propofol on endothelium-dependent relaxation (induced by substance P) were studied in human omental arteries and veins. Propofol, at a clinically relevant concentration, was found to promote endothelium-dependent relaxation mediated via hyperpolarization in human omental arteries and via both nitric oxide and hyperpolarization in human omental veins. The effects of sevoflurane on sympathetic neurotransmission were studied in human omental arteries and veins. We found that sevoflurane depresses the sympathetic neuromuscular transmission by lowering the neuronal noradrenaline release and noradrenaline sensitivity in the arteries and by lowering the noradrenaline release in the veins. The effects of sevoflurane on endothelium-dependent relaxation (induced by substance P) were studied in human omental arteries and veins. Sevoflurane was found to promote endothelium-dependent relaxation in human omental arteries and veins probably via an enhancement of the response of smooth muscle cells to relaxing mediators.

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