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Naloxone Antagonizes Soman‐induced Central Respiratory Depression in Rats
Author(s) -
Škrbić Ranko,
Stojiljković Miloš P.,
Ćetković Slavko S.,
Dobrić Silva,
Jeremić Dejan,
Vulović Maja
Publication year - 2017
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/bcpt.12745
Subject(s) - (+) naloxone , soman , pharmacology , muscarinic acetylcholine receptor , anesthesia , atropine , respiratory system , phrenic nerve , opioidergic , medicine , stimulation , muscarine , chemistry , endocrinology , antagonist , receptor , biochemistry , acetylcholinesterase , enzyme
The influence of naloxone on respiration impaired by the highly toxic organophosphate nerve agent soman in anaesthetized rats was investigated. Soman, administered in a dose that was ineffective in blocking the electrically induced contractions of the phrenic nerve‐diaphragm preparation in situ , induced a complete block of the spontaneous respiratory movements of the diaphragm, indicating the domination of central over the peripheral effects. Naloxone dose‐dependently antagonized the soman‐induced respiratory blockade. Atropine, at a dose that was per se ineffective in counteracting soman‐induced respiratory depression, potentiated the protective effects of naloxone and completely restored respiration. Naloxone remained completely ineffective in antagonizing respiratory depression induced by the muscarinic receptor agonist the oxotremorine. It is assumed that naloxone antagonizes soman‐induced respiratory inhibition by blocking endogenous opioidergic respiratory control pathways that are independent of the stimulation of muscarinic receptors.