Activation of the supraspinal pain inhibition system by ketamine hydrochloride.
The neurophysiologic mechanism of ketamine-induced analgesia was studied in cats under conditions of electrolytic decerebration or pentobarbital anesthesia. Injection of bradykinin into the femoral artery served as the noxious stimulus and the neural response in the lateral funiculus of the spinal cord was recorded by the multi-unit activity technique. Ketamine depressed the bradykinin-induced response more markedly in decerebrate, non-anesthetized cats than in pentobarbital-anesthetized cats. The depressant action disappeared following cervical cord transection at C1, in both decerebrate non-anesthetized and pentobarbital-anesthetized cats. Thus the analgesic action of ketamine is probably exerted mainly through activation of the supraspinal pain inhibition system and a direct action on the spinal cord nociceptive neural mechanism, if any, is slight. The excitatory action of ketamine on the supraspinal pain inhibition system is susceptible to the depressant action of pentobarbital.
D000818:Animals; D001920:Bradykinin / Q000008:administration & dosage; D002415:Cats; D003655:Decerebrate State / Q000503:physiopathology; D005260:Female; D007649:Ketamine / Q000494:pharmacology*; D008297:Male; D010146:Pain / Q000503:physiopathology*; D010424:Pentobarbital / Q000494:pharmacology; D013116:Spinal Cord / Q000187:drug effects / Q000502:physiology*
D007649:Ketamine; D010424:Pentobarbital; D001920:Bradykinin