Acute pathophysiological processes after ischaemic and traumatic brain injury

被引:119
作者
Kunz, Alexander [1 ,2 ]
Dirnagl, Ulrich [1 ,2 ]
Mergenthaler, Philipp [1 ,2 ]
机构
[1] Charite Univ Med Berlin, Ctr Stroke Res Berlin, Dept Neurol, Charitepl 1, D-10117 Berlin, Germany
[2] Charite Univ Med Berlin, Ctr Stroke Res Berlin, Dept Expt Neurol, D-10117 Berlin, Germany
关键词
brain ischaemia; ischaemic stroke; traumatic brain injury; penumbra; excitotoxicity; peri-infarct depolarization; apoptosis; inflammation; brain edema;
D O I
10.1016/j.bpa.2010.10.001
中图分类号
R614 [麻醉学];
学科分类号
100217 ;
摘要
Ischaemic stroke and brain trauma are among the leading causes of mortality and long-term disability in the western world. Enormous endeavours have been made to elucidate the complex pathophysiology of ischaemic and traumatic brain injury with the intention of developing new therapeutic strategies for patients suffering from these devastating diseases. This article reviews the current knowledge on cascades that are activated after ischaemic and traumatic brain injury and that lead to progression of tissue damage. Main attention will be on pathophysiological events initiated after ischaemic stroke including excitotoxicity, oxidative/ nitrosative stress, peri-infarct depolarizations, apoptosis and inflammation. Additionally, specific pathophysiological aspects after traumatic brain injury will be discussed along with their similarities and differences to ischaemic brain injury. This article provides prerequisites for understanding the therapeutic strategies for stroke and trauma patients which are addressed in other articles of this issue. (C) 2010 Elsevier Ltd. All rights reserved.
引用
收藏
页码:495 / 509
页数:15
相关论文
共 145 条
[101]  
Minghetti Luisa, 2007, Subcell Biochem, V42, P127
[102]   Matrix metalloproteinase expression after human cardioembolic stroke -: Temporal profile and relation to neurological impairment [J].
Montaner, J ;
Alvarez-Sabín, J ;
Molina, C ;
Anglés, A ;
Abilleira, S ;
Arenillas, J ;
González, MA ;
Monasterio, J .
STROKE, 2001, 32 (08) :1759-1766
[103]   Experimental models of traumatic brain injury: Do we really need to build a better mousetrap? [J].
Morales, DM ;
Marklund, N ;
Lebold, D ;
Thompson, HJ ;
Pitkanen, A ;
Maxwell, WL ;
Longhi, L ;
Laurer, H ;
Maegele, M ;
Neugebauer, E ;
Graham, DI ;
Stocchetti, N ;
McIntosh, TK .
NEUROSCIENCE, 2005, 136 (04) :971-989
[104]   Nitric oxide, ischaemia and brain inflammation [J].
Murphy, S. ;
Gibson, C. L. .
BIOCHEMICAL SOCIETY TRANSACTIONS, 2007, 35 :1133-1137
[105]   Delayed treatment with aminoguanidine decreases focal cerebral ischemic damage and enhances neurologic recovery in rats [J].
Nagayama, M ;
Zhang, FY ;
Iadecola, C .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1998, 18 (10) :1107-1113
[106]   The cyclooxygenase-2 inhibitor NS-398 ameliorates ischemic brain injury in wild-type mice but not in mice with deletion of the inducible nitric oxide synthase gene [J].
Nagayama, M ;
Niwa, K ;
Nagayama, T ;
Ross, ME ;
Iadecola, C .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1999, 19 (11) :1213-1219
[107]  
Nakamura H, 2010, BRAIN
[108]  
NAMURA S, 1998, THE JOURNAL OF NEURO, V15, P3659
[109]   CHARACTERIZATION OF CORTICAL DEPOLARIZATIONS EVOKED IN FOCAL CEREBRAL-ISCHEMIA [J].
NEDERGAARD, M ;
HANSEN, AJ .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1993, 13 (04) :568-574
[110]   Excitotoxins in neuronal apoptosis and necrosis [J].
Nicotera, P ;
Lipton, SA .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1999, 19 (06) :583-591