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- W2040226041 abstract "Dextromoramide (0.01−0.2 mg/kg i.v.) and fentanyl (0.005−0.05 mg/kg) induced a dose dependent decrease in blood pressure and heart rate in dogs. These effects appear to be to a centrally mediated decrease in sympathetic tone, (i) Both drugs are 10−20 times more potent when injected into the vertebral artery or the cisterna magna than when they were injected intravanously, (ii) Both drugs reduced splanchnic nerve activity in intact animals. The effect appears to be localized to the medulla oblongata as suggested by central injections; transection of the brain stem at midpoint levels did not change the effects on blood pressure and heart rate induced by dextromoramide in intact bivagotomized dogs. After transection of the spinal cord at C1, dextromoramide induced a strong decrease in heart rate and a hypertension. Cutting of both vagus nerves abolished the decrease in heart rate and blood pressure. The hypotensive effect was therefore due to the bradycardia reducing cardiac output. In contrast in intact and midpontine dogs, a reduction in sympathetic tone contributes to the hypothensive effect. Nalorphine prevented and reversed the hypotensive, bradycardic and sympatho-inhibitory effects of dextromoramide. Piperoxan and yohimbine, two potent peripheral and central α-adrenoceptor blocking agents did not change the effects of dextromoramide. However oxotremorine or acetylcholine administered into the cisterna magna and vertebral artery administration of physostigmine abolished or reversed the haemodynamic effects of dextromoramide. A tropine abolished the antagonistic effects of cholinomimetic agents on the central cardiovascular effects of dextromoramide. Muscarinic mechanism appear to be involved in the haemodynamic effects of analgesic agents." @default.
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- W2040226041 title "Centrally mediated bradycardia and hypotension induced by narcotic analgesics: Dextromoramide and fentanyl" @default.
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- W2040226041 doi "https://doi.org/10.1016/0014-2999(74)90113-7" @default.
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