Sequelae following traumatic brain injury - The cerebrovascular perspective

被引:79
作者
Golding, EM [1 ]
机构
[1] Baylor Coll Med, Dept Anesthesiol, Houston, TX 77030 USA
关键词
cerebrovasculature; traumatic brain injury; autoregulation;
D O I
10.1016/S0165-0173(02)00141-8
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Traumatic brain injury (TBI) initiates a huge repertoire of biochemical perturbations. On one hand, destructive events are set into motion while on the other hand, protective and recovery mechanisms are evoked, each with their own temporal and spatial characteristics. The brain exists as a finely tuned balance between vascular, neuronal and glial interactions and so a complex interplay between these factors will dictate the final evolution of pathogenesis. Although vascular damage is a key event, it remains a somewhat neglected component to the underlying degenerative processes that evolve following injury to the brain. The present review will act to integrate the current knowledge of the vascular events proceeding injury to the brain, with an emphasis on how this impacts the: control of vascular function and thus cerebral blood flow. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:377 / 388
页数:12
相关论文
共 154 条
[101]   AGENTS THAT MODIFY EDRF FORMATION ALTER ANTIPLATELET PROPERTIES OF BRAIN ARTERIOLAR ENDOTHELIUM INVIVO [J].
NISHIMURA, H ;
ROSENBLUM, WI ;
NELSON, GH ;
BOYNTON, S .
AMERICAN JOURNAL OF PHYSIOLOGY, 1991, 261 (01) :H15-H21
[102]   Prolonged activation of NF-κB following traumatic brain injury in rats [J].
Nonaka, M ;
Chen, XH ;
Pierce, JES ;
Leoni, MJ ;
McIntosh, TK ;
Wolf, JA ;
Smith, DH .
JOURNAL OF NEUROTRAUMA, 1999, 16 (11) :1023-1034
[103]   LARGE APPARENT WORK CAPABILITY OF BLOOD-BRAIN-BARRIER - STUDY OF MITOCHONDRIAL CONTENT OF CAPILLARY ENDOTHELIAL CELLS IN BRAIN AND OTHER TISSUES OF RAT [J].
OLDENDORF, WH ;
CORNFORD, ME ;
BROWN, WJ .
ANNALS OF NEUROLOGY, 1977, 1 (05) :409-417
[104]   THE EFFECT OF P-CHLOROPHENYLALANINE ON CEREBRAL METABOLISM AND BIOGENIC-AMINE CONTENT OF TRAUMATIZED BRAIN [J].
PAPPIUS, HM ;
DADOUN, R ;
MCHUGH, M .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1988, 8 (03) :324-334
[105]   Chronic metabolic sequelae of traumatic brain injury: prolonged suppression of somatosensory activation [J].
Passineau, MJ ;
Zhao, W ;
Busto, R ;
Dietrich, WD ;
Alonso, O ;
Loor, JY ;
Bramlett, HM ;
Ginsberg, MD .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2000, 279 (03) :H924-H931
[106]   PROSTACYCLIN, INDOMETHACIN AND THE CEREBRAL-CIRCULATION [J].
PICKARD, J ;
TAMURA, A ;
STEWART, M ;
MCGEORGE, A ;
FITCH, W .
BRAIN RESEARCH, 1980, 197 (02) :425-431
[107]   INTERACTIONS OF LYMPHOCYTES-T WITH HUMAN VASCULAR ENDOTHELIAL-CELLS - ROLE OF ENDOTHELIAL-CELLS SURFACE-ANTIGENS [J].
POBER, JS ;
GIMBRONE, MA ;
COLLINS, T ;
COTRAN, RS ;
AULT, KA ;
FIERS, W ;
KRENSKY, AM ;
CLAYBERGER, C ;
REISS, CS ;
BURAKOFF, SJ .
IMMUNOBIOLOGY, 1984, 168 (3-5) :483-494
[108]   VASCULAR-PERMEABILITY ALTERATIONS TO HORSERADISH-PEROXIDASE IN EXPERIMENTAL BRAIN INJURY [J].
POVLISHOCK, JT ;
BECKER, DP ;
SULLIVAN, HG ;
MILLER, JD .
BRAIN RESEARCH, 1978, 153 (02) :223-239
[109]  
Ragnarsson KT, 1999, JAMA-J AM MED ASSOC, V282, P974
[110]  
Reivich M, 1974, Res Publ Assoc Res Nerv Ment Dis, V53, P125