[Brain protection by anesthetics].
Many investigators have attempted to protect the brain against ischemia by reducing the cerebral metabolic rate using anesthetic agents. However, the magnitude of suppression of the cerebral metabolic rate does not correlate with neuroprotective effects of anesthetics, suggesting that other factors besides reduction in the cerebral metabolic rate contribute to the protection. Facilitation of protein synthesis, GABAergic activity, and anti-oxidant action are likely factors responsible for beneficial effects of barbiturates and propofol. Although the brain is protected during anesthesia, anesthetics cannot provide effects sufficiently enough to recover damage caused by severe ischemia. Further, no desired outcome has been reported by treatments after ischemic events.
Adachi
Naoto
N
Medical Division, Mabuchi Clinic, Kyoto 600-8357.
D000777:Anesthetics / Q000494:pharmacology*; D018685:Anesthetics, Inhalation / Q000494:pharmacology; D000779:Anesthetics, Local / Q000494:pharmacology; D017209:Apoptosis; D001921:Brain / Q000378:metabolism* / Q000473:pathology; D002545:Brain Ischemia / Q000517:prevention & control*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002560:Cerebrovascular Circulation; D004734:Energy Metabolism; D006801:Humans; D018696:Neuroprotective Agents / Q000494:pharmacology*
D000777:Anesthetics; D018685:Anesthetics, Inhalation; D000779:Anesthetics, Local; D002121:Calcium Channel Blockers; D018696:Neuroprotective Agents