The impact of anesthetics and hyperoxia on cortical spreading depression

被引:84
作者
Kudo, Chiho [1 ]
Nozari, Ala [1 ,2 ]
Moskowitz, Michael A. [1 ]
Ayata, Cenk [1 ,3 ,4 ]
机构
[1] Harvard Univ, Massachusetts Gen Hosp, Sch Med,Dept Radiol, Stroke Neurovasc Regulat Lab, Boston, MA 02129 USA
[2] Harvard Univ, Massachusetts Gen Hosp, Sch Med,Dept Neurol, Dept Anesthesia & Crit Care, Boston, MA 02129 USA
[3] Harvard Univ, Massachusetts Gen Hosp, Sch Med,Dept Neurol, Stroke Serv, Boston, MA 02129 USA
[4] Harvard Univ, Massachusetts Gen Hosp, Sch Med,Dept Neurol, Neurosci Intens Care Unit, Boston, MA 02129 USA
关键词
isoflurane; alpha-chloralose; urethane; nitrous oxide; electrophysiology;
D O I
10.1016/j.expneurol.2008.03.026
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Cortical spreading depression (CSD), a transient neuronal and glial depolarization that propagates slowly across the cerebral cortex, is the putative electrophysiological event underlying migraine aura. It negatively impacts tissue injury during stroke, cerebral contusion and intracranial hemorrhage. Susceptibility to CSD has been assessed in several experimental animal models in vivo, such as after topical KCl application or cathodal stimulation. Various combinations of anesthetics and ambient conditions have been used by different laboratories making comparisons problematic and differences in data difficult to reconcile. We systematically studied CSD susceptibility comparing commonly used experimental anesthetics (isoflurane, alpha-chloralose, and urethane) with or without N2O or normobaric hyperoxia (100% O-2 inhalation). The frequency of evoked CSDs, and their propagation speed, duration, and amplitude were recorded during 2 h topical KCl (1 M) application. We found that N2O reduced CSD frequency when combined with isoflurane or urethane, but not (x-chloralose; N2O also decreased CSD propagation speed and duration. Urethane anesthesia was associated with the highest CSD frequency that was comparable to pentobarbital. Inhalation Of 100% O-2 did not alter CSD frequency, propagation speed or duration in combination with any of the anesthetics tested. Our data show anesthetic modulation of CSD susceptibility in an experimental model of human disease, underscoring the importance of proper study design for hypothesis testing as well as for comparing results between studies. (C) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:201 / 206
页数:6
相关论文
共 44 条
[1]   Suppression of cortical spreading depression in migraine prophylaxis [J].
Ayata, C ;
Jin, HW ;
Kudo, C ;
Dalkara, T ;
Moskowitz, MA .
ANNALS OF NEUROLOGY, 2006, 59 (04) :652-661
[2]   Context-sensitive half-times and other decrement times of inhaled anesthetics [J].
Bailey, JM .
ANESTHESIA AND ANALGESIA, 1997, 85 (03) :681-686
[3]   Pharmacological modulation of the refractory period of retinal spreading depression [J].
Brand, S ;
de Lima, VMF ;
Hanke, W .
NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY, 1998, 357 (04) :419-425
[4]   Drug therapy: Mechanisms of actions of inhaled anesthetics [J].
Campagna, JA ;
Miller, KW ;
Forman, SA .
NEW ENGLAND JOURNAL OF MEDICINE, 2003, 348 (21) :2110-2124
[5]   GENERAL-ANESTHETICS INHIBIT THE RESPONSES INDUCED BY GLUTAMATE RECEPTOR AGONISTS IN THE MOUSE CORTEX [J].
CARLA, V ;
MORONI, F .
NEUROSCIENCE LETTERS, 1992, 146 (01) :21-24
[6]   Competitive inhibition at the glycine site of the n-methyl-d-aspartate receptor by the Anesthetics xenon and Isoflurane [J].
Dickinson, Robert ;
Peterson, Brian K. ;
Banks, Paul ;
Simillis, Constandhos ;
Martin, Juan Carlos Sacristan ;
Valenzuela, Cados A. ;
Maze, Mervyn ;
Franks, Nicholas P. .
ANESTHESIOLOGY, 2007, 107 (05) :756-767
[7]  
ELBEHEIRY H, 1989, EXP BRAIN RES, V77, P87
[8]   The TREK K2P channels and their role in general anaesthesia and neuroprotection [J].
Franks, NP ;
Honoré, E .
TRENDS IN PHARMACOLOGICAL SCIENCES, 2004, 25 (11) :601-608
[9]  
Garrett KM, 1998, J PHARMACOL EXP THER, V285, P680
[10]   KETAMINE BLOCKADE OF CORTICAL SPREADING DEPRESSION IN RATS [J].
GORELOVA, NA ;
KOROLEVA, VI ;
AMEMORI, T ;
PAVLIK, V ;
BURES, J .
ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY, 1987, 66 (04) :440-447