Ischemic tolerance and endogenous neuroprotection

被引:671
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
    Alkayed, NJ
    Goyagi, T
    Joh, HD
    Klaus, J
    Harder, DR
    Traystman, RJ
    Hurn, PD
    [J]. 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
    Barone, FC
    White, RF
    Spera, PA
    Ellison, J
    Currie, RW
    Wang, XK
    Feuerstein, GZ
    [J]. 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
    Bernaudin, M
    Nedelec, AS
    Divoux, D
    MacKenzie, ET
    Petit, E
    Schumann-Bard, P
    [J]. 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
    Blondeau, N
    Widmann, C
    Lazdunski, M
    Heurteaux, C
    [J]. NEUROSCIENCE, 2002, 109 (02) : 231 - 241
  • [7] The late phase of preconditioning
    Bolli, R
    [J]. CIRCULATION RESEARCH, 2000, 87 (11) : 972 - 983
  • [8] Increase in endogenous brain superoxide dismutase as a potential mechanism of lipopolysaccharide-induced brain ischemic tolerance
    Bordet, R
    Deplanque, D
    Maboudou, P
    Puisieux, F
    Pu, Q
    Robin, E
    Martin, A
    Bastide, M
    Leys, D
    Lhermitte, M
    Dupuis, B
    [J]. 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
    Chang, J
    Knowlton, AA
    Wasser, JS
    [J]. 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
    Chen, DX
    Minami, M
    Henshall, DC
    Meller, R
    Kisby, G
    Simon, RP
    [J]. JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 2003, 23 (01) : 88 - 98