A neurochemical hypothesis for halothane anesthesia.
We hypothesize that anesthetic agents exert their effects through an inhibition of oxidation of reduced nicotinamide adenine dinucleotide (NADH) in the synaptic regions of the brain. This inhibition could lead to gamma-amino-butyric acid (GABA) accumulation in the synaptic cleft and to hyperpolarization of the post-synaptic membrane. The resulting reduction in synaptic transmission then would manifest itself as the anesthetic state, reducing the work performed by the brain so that cerebral respiration is reduced and cerebral metabolite energy is conserved.
D000085:Acetates / Q000378:metabolism; D000109:Acetylcholine / Q000378:metabolism; D000769:Anesthesia, Inhalation; D000818:Animals; D002250:Carbon Radioisotopes; D002540:Cerebral Cortex / Q000187:drug effects / Q000378:metabolism; D006221:Halothane / Q000494:pharmacology*; D066298:In Vitro Techniques; D009243:NAD / Q000378:metabolism; D009448:Neurochemistry; D010101:Oxygen Consumption / Q000187:drug effects; D011773:Pyruvates / Q000378:metabolism; D051381:Rats; D009435:Synaptic Transmission / Q000187:drug effects; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D000085:Acetates; D002250:Carbon Radioisotopes; D011773:Pyruvates; D009243:NAD; D005680:gamma-Aminobutyric Acid; D000109:Acetylcholine; D006221:Halothane