Influence of glucose (in vivo or in vitro) on duration of narcotic analgesics and on the kinetics of drug metabolism.
The duration of analgesia of the narcotics, methadone, morphine and codeine was prolonged by glucose treatment. This prolongation was associated with a decrease in in vitro metabolism of the narcotics. Chlorpromazine metabolism was not significantly inhibited by glucose treatment, indicating that glucose exerts some selectivity in the extent to which it inhibits various oxidative metabolic pathways. Michaelis-Menten type kinetics showed a mixed type of competitive and noncompetitive inhibition of methadone metabolism upon oral administration of glucose or in vitro addition of glucose to an enzyme system prepared from mouse liver. Other factors may be involved, such as the possibility that glucose might increase the permeability of the brain to barbiturate. However, in glucose-treated mice decreased metabolism of the barbiturate and narcotics seemed to be the major factor in the prolongation of their duration of action.
D000701:Analgesics, Opioid / Q000378:metabolism / Q000494:pharmacology*; D000818:Animals; D002746:Chlorpromazine / Q000378:metabolism; D003061:Codeine / Q000494:pharmacology; D004347:Drug Interactions; D005947:Glucose / Q000494:pharmacology*; D007700:Kinetics; D008297:Male; D008614:Meperidine / Q000494:pharmacology; D051379:Mice; D009020:Morphine / Q000494:pharmacology; D004364:Pharmaceutical Preparations / Q000378:metabolism*; D013997:Time Factors
D000701:Analgesics, Opioid; D004364:Pharmaceutical Preparations; D009020:Morphine; D008614:Meperidine; D005947:Glucose; D002746:Chlorpromazine; D003061:Codeine