Mutation of KCNK5 or kir3.2 potassium channels in mice does not change minimum alveolar anesthetic concentration

被引:30
作者
Gerstin, KM [1 ]
Gong, DH [1 ]
Abdallah, M [1 ]
Winegar, BD [1 ]
Eger, EI [1 ]
Gray, AT [1 ]
机构
[1] Univ Calif San Francisco, San Francisco Gen Hosp, Dept Anesthesia & Perioperat Care, San Francisco, CA 94110 USA
关键词
D O I
10.1213/01.ANE.0000056921.15974.EC
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
Several reports suggest that clinically used concentrations of inhaled anesthetics can increase conductance through noninactivating potassium channels and that the resulting hyperpolarization might decrease excitability, thereby leading to the anesthetic state. We speculated that animals deficient in such potassium channels might be resistant to the effects of anesthetics. Thus, in the present study, we measured the minimum alveolar anesthetic concentration (MAC) needed to prevent movement in response to a noxious stimulus in 50% of adult mice lacking functional KCNK5 potassium channel subunits and compared these results with those for heterozygous and wild-type mice. We also measured MAC in weaver mice that had a mutation in the potassium channel Kir3.2 and compared the resulting values with those for wild-type mice. MAC values for desflurane, halothane, and isoflurane for KCNK5-deficient mice and isoflurane MAC values for weaver mice did not differ from MAC values found in control mice. Our results do not support the notion that these potassium channels mediate the capacity of inhaled anesthetics to produce immobility. In addition, we found that the weaver mice did not differ from control mice in their susceptibility to convulsions from the nonimmobilizers flurothyl [di-(2,2,2,-trifluoroethyl)ether] or 2N (1,2-dichlorohexafluorocyclobutane).
引用
收藏
页码:1345 / 1349
页数:5
相关论文
共 20 条
[1]   EXAGGERATED ANESTHETIC REQUIREMENTS IN THE PREFERENTIALLY ANESTHETIZED BRAIN [J].
ANTOGNINI, JF ;
SCHWARTZ, K .
ANESTHESIOLOGY, 1993, 79 (06) :1244-1249
[2]   Behavioral phenotypes of inbred mouse strains: implications and recommendations for molecular studies [J].
Crawley, JN ;
Belknap, JK ;
Collins, A ;
Crabbe, JC ;
Frankel, W ;
Henderson, N ;
Hitzemann, RJ ;
Maxson, SC ;
Miner, LL ;
Silva, AJ ;
Wehner, JM ;
WynshawBoris, A ;
Paylor, R .
PSYCHOPHARMACOLOGY, 1997, 132 (02) :107-124
[3]   NARCOTIC PROPERTIES OF CARBON DIOXIDE IN DOG [J].
EISELE, JH ;
EGER, EI ;
MUALLEM, M .
ANESTHESIOLOGY, 1967, 28 (05) :856-&
[4]   TONIC CLONIC SEIZURES IN A MOUSE MUTANT CARRYING THE WEAVER GENE [J].
EISENBERG, B ;
MESSER, A .
NEUROSCIENCE LETTERS, 1989, 96 (02) :168-172
[5]   Localization of the tandem pore domain K+ channel KCNK5 (TASK-2) in the rat central nervous system [J].
Gabriel, A ;
Abdallah, M ;
Yost, CS ;
Winegar, BD ;
Kindler, CH .
MOLECULAR BRAIN RESEARCH, 2002, 98 (1-2) :153-163
[6]   TOK1 is a volatile anesthetic stimulated K+ channel [J].
Gray, AT ;
Winegar, BD ;
Leonoudakis, DJ ;
Forsayeth, JR ;
Yost, CS .
ANESTHESIOLOGY, 1998, 88 (04) :1076-1084
[7]   Volatile anesthetics activate the human tandem pore domain baseline K+ channel KCNK5 [J].
Gray, AT ;
Zhao, BB ;
Kindler, CH ;
Winegar, BD ;
Mazurek, MJ ;
Xu, J ;
Chavez, RA ;
Forsayeth, JR ;
Yost, CS .
ANESTHESIOLOGY, 2000, 92 (06) :1722-1730
[8]  
Karschin C, 1996, J NEUROSCI, V16, P3559
[9]   Distribution analysis of human two pore domain potassium channels in tissues of the central nervous system and periphery [J].
Medhurst, AD ;
Rennie, G ;
Chapman, CG ;
Meadows, H ;
Duckworth, MD ;
Kelsell, RE ;
Gloger, II ;
Pangalos, MN .
MOLECULAR BRAIN RESEARCH, 2001, 86 (1-2) :101-114
[10]   Inhalational anesthetics activate two-pore-domain background K+ channels [J].
Patel, AJ ;
Honoré, E ;
Lesage, F ;
Fink, M ;
Romey, G ;
Lazdunski, M .
NATURE NEUROSCIENCE, 1999, 2 (05) :422-426