Ischemic tolerance and endogenous neuroprotection

被引:678
作者
Dirnagl, U [1 ]
Simon, RP
Hallenbeck, JM
机构
[1] Humboldt Univ, Charite Hosp, D-10098 Berlin, Germany
[2] RS Dow Neurobiol Labs, Portland, OR 97232 USA
[3] NINDS, Stroke Branch, NIH, Bethesda, MD 20892 USA
关键词
D O I
10.1016/S0166-2236(03)00071-7
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Practically any stimulus capable of causing injury to a tissue or organ can, when applied close to (but below) the threshold of damage, activate endogenous protective mechanisms - thus potentially lessening the impact of subsequent, more severe stimuli. A sub-threshold ischemic insult applied to the brain, for example, activates certain cellular pathways that can help to reduce damage caused by subsequent ischemic episodes - a phenomenon known as 'ischemic preconditioning' (IP) or 'ischemic tolerance' (IT). Although investigated for some time in model organisms, IP/IT has recently been shown in human brain. This opens a window into endogenous neuroprotection and, potentially, a window of opportunity to utilize these mechanisms in the clinic to treat patients with stroke and other CNS disorders.
引用
收藏
页码:248 / 254
页数:7
相关论文
共 76 条
[1]   Neuroprotection and P4502C11 upregulation after experimental transient ischemic attack [J].
Alkayed, NJ ;
Goyagi, T ;
Joh, HD ;
Klaus, J ;
Harder, DR ;
Traystman, RJ ;
Hurn, PD .
STROKE, 2002, 33 (06) :1677-1684
[2]   Ischemic preconditioning and brain tolerance - Temporal histological and functional outcomes, protein synthesis requirement, and interleukin-1 receptor antagonist and early gene expression [J].
Barone, FC ;
White, RF ;
Spera, PA ;
Ellison, J ;
Currie, RW ;
Wang, XK ;
Feuerstein, GZ .
STROKE, 1998, 29 (09) :1937-1950
[3]   Normobaric hypoxia induces tolerance to focal permanent cerebral ischemia in association with an increased expression of hypoxia-inducible factor-1 and its target genes, erythropoietin and VEGF, in the adult mouse brain [J].
Bernaudin, M ;
Nedelec, AS ;
Divoux, D ;
MacKenzie, ET ;
Petit, E ;
Schumann-Bard, P .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2002, 22 (04) :393-403
[4]  
Bickler PE, 2002, NEUROSCIENTIST, V8, P234
[5]  
Bickler PE, 2002, J EXP BIOL, V205, P3579
[6]   Polyunsaturated fatty acids induce ischemic and epileptic tolerance [J].
Blondeau, N ;
Widmann, C ;
Lazdunski, M ;
Heurteaux, C .
NEUROSCIENCE, 2002, 109 (02) :231-241
[7]   The late phase of preconditioning [J].
Bolli, R .
CIRCULATION RESEARCH, 2000, 87 (11) :972-983
[8]   Increase in endogenous brain superoxide dismutase as a potential mechanism of lipopolysaccharide-induced brain ischemic tolerance [J].
Bordet, R ;
Deplanque, D ;
Maboudou, P ;
Puisieux, F ;
Pu, Q ;
Robin, E ;
Martin, A ;
Bastide, M ;
Leys, D ;
Lhermitte, M ;
Dupuis, B .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2000, 20 (08) :1190-1196
[9]   Expression of heat shock proteins in turtle and mammal hearts: relationship to anoxia tolerance [J].
Chang, J ;
Knowlton, AA ;
Wasser, JS .
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 2000, 278 (01) :R209-R214
[10]   Upregulation of mitochondrial base-excision repair capability within rat brain after brief ischemia [J].
Chen, DX ;
Minami, M ;
Henshall, DC ;
Meller, R ;
Kisby, G ;
Simon, RP .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2003, 23 (01) :88-98