Studies on a central site of action for naloxone in endotoxin shock.
A complete understanding of naloxone's role in shock has not been well established; however, it has been accepted that naloxone applied specifically to the central nervous system can improve the course of the cardiovascular response. The currently available data would suggest that these central effects are mediated via nuclei that 1) are found in both the rostral and caudal regions of the brainstem, 2) contain opiate receptors, 3) interact with the fastigial nuclei of the cerebellum, and 4) possibly receive input from peripheral thermoreceptors. Recordings of neural activity from specific nuclei during shock as well as microinjections and iontophoresis of naloxone onto specific sites is needed to improve the current understanding of this apparently complex process.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D001923:Brain Chemistry / Q000187:drug effects*; D001933:Brain Stem / Q000187:drug effects / Q000503:physiopathology; D002531:Cerebellum / Q000187:drug effects / Q000503:physiopathology; D004285:Dogs; D000882:Haplorhini; D009270:Naloxone / Q000494:pharmacology*; D009292:Narcotic Antagonists / Q000494:pharmacology*; D010275:Parasympathetic Nervous System / Q000503:physiopathology; D011817:Rabbits; D051381:Rats; D011957:Receptors, Opioid / Q000187:drug effects; D012772:Shock, Septic / Q000188:drug therapy* / Q000503:physiopathology
D009292:Narcotic Antagonists; D011957:Receptors, Opioid; D009270:Naloxone