Anesthetic-mediated protection/preconditioning during cerebral ischemia.
Cerebral ischemia is a multi-faceted neurodegenerative pathology that causes cellular injury to neurons within the central nervous system. In light of the underlying mechanisms being elucidated, clinical trials to find possible neuroprotectants to date have failed, thus highlighting the need for new putative targets to offer protection. Recent evidence has clearly shown that anesthetics can confer significant protection and or induce a preconditioning effect against cerebral ischemia-induced injury. This review will focus on the putative protection/preconditioning that is afforded by anesthetics, their possible interaction with GABA(A) and glutamate receptors and two-pore potassium channels. In addition, the interaction with inflammatory, apoptotic and underlying molecular (particularly immediately early genes and inducible nitric oxide synthase etc) pathways, the activation of K(ATP) channels and the ability to provide lasting protection will also be addressed.
Clarkson
Andrew N
AN
Department of Anatomy and Structural Biology, University of Otago, PO Box 913, Dunedin 9054, New Zealand. andrew.clarkson@stonebow.otago.ac.nz
D018685:Anesthetics, Inhalation / Q000494:pharmacology*; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D002545:Brain Ischemia / Q000378:metabolism / Q000517:prevention & control*; D004195:Disease Models, Animal; D006801:Humans; D019194:Ischemic Preconditioning / Q000379:methods*; D018696:Neuroprotective Agents / Q000494:pharmacology*; D024683:Potassium Channels, Tandem Pore Domain / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017470:Receptors, Glutamate / Q000187:drug effects / Q000378:metabolism; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
D018685:Anesthetics, Inhalation; D018696:Neuroprotective Agents; D024683:Potassium Channels, Tandem Pore Domain; D017470:Receptors, Glutamate; D005680:gamma-Aminobutyric Acid