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Methoctramine, a cardioselective muscarinic cholinergic antagonist, prevents fentanyl‐induced bradycardia in the dog
Author(s) -
HENDRIX P.K.,
ROBINSON E.P.,
RAFFE M.R.
Publication year - 1995
Publication title -
journal of veterinary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.527
H-Index - 60
eISSN - 1365-2885
pISSN - 0140-7783
DOI - 10.1111/j.1365-2885.1995.tb00560.x
Subject(s) - methoctramine , bradycardia , fentanyl , medicine , anesthesia , muscarinic acetylcholine receptor , antagonist , tachycardia , muscarinic acetylcholine receptor m2 , heart rate , blood pressure , receptor
A controlled study examining the effects of the cardioselective muscarinic cholinergic antagonist methoctramine on fentanyl‐induced bradycardia was performed in six dogs. Five doses of methoctramine (6, 10, 20, 30 and 60 |ig/kg) followed by fentanyl (20 μg/kg) were administered randomly on separate days. Fentanyl caused a significant reduction in heart rate from baseline values. Moreover, fentanyl produced a variety of arrhythmogenic actions indicative of vagal hyper‐activity, including sinus bradycardia, second‐degree atrioventricular block and ventricular and supraventricular escape beats. Administration of methoctramine 5 min before fentanyl injection prevented the bradycardic effects of fentanyl in a dose‐dependent manner, with high doses of methoctramine causing sinus tachycardia. Using regression analysis, the dose of methoctramine necessary to prevent fentanyl‐induced bradyarrhythmias without causing tachycardia was calculated as 14.4 μg/kg. The study confirmed that fentanyl administration in the conscious dog causes profound bradycardia with bradyarrhythmias. The cardioselective muscarinic antagonist agent methoctramine prevented the bradycardic effects of fentanyl.