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
[1]   Inhibition of brain P-450 arachidonic acid epoxygenase decreases baseline cerebral blood flow [J].
Alkayed, NJ ;
Birks, EK ;
Hudetz, AG ;
Roman, RJ ;
Henderson, L ;
Harder, DR .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1996, 271 (04) :H1541-H1546
[2]   PREDOMINANT LOCALIZATION IN GLIAL-CELLS OF FREE L-ARGININE - IMMUNOCYTOCHEMICAL EVIDENCE [J].
AOKI, E ;
SEMBA, R ;
MIKOSHIBA, K ;
KASHIWAMATA, S .
BRAIN RESEARCH, 1991, 547 (02) :190-192
[3]   Role of endothelin in pial artery vasoconstriction and altered responses to vasopressin after brain injury [J].
Armstead, WM .
JOURNAL OF NEUROSURGERY, 1996, 85 (05) :901-907
[4]   Brain injury impairs prostaglandin cerebrovasodilation [J].
Armstead, WM .
JOURNAL OF NEUROTRAUMA, 1998, 15 (09) :721-729
[5]   Temporal profile and cell subtype distribution of activated caspase-3 following experimental traumatic brain injury [J].
Beer, R ;
Franz, G ;
Srinivasan, A ;
Hayes, RL ;
Pike, BR ;
Newcomb, JK ;
Zhao, X ;
Schmutzhard, E ;
Poewe, W ;
Kampfl, A .
JOURNAL OF NEUROCHEMISTRY, 2000, 75 (03) :1264-1273
[6]   NITRIC-OXIDE - A PHYSIOLOGICAL MESSENGER MOLECULE [J].
BREDT, DS ;
SNYDER, SH .
ANNUAL REVIEW OF BIOCHEMISTRY, 1994, 63 :175-195
[7]   REGIONAL CEREBRAL BLOOD-FLOW AFTER CONTROLLED CORTICAL IMPACT INJURY IN RATS [J].
BRYAN, RM ;
CHERIAN, L ;
ROBERTSON, C .
ANESTHESIA AND ANALGESIA, 1995, 80 (04) :687-695
[8]   Traumatic brain injury does not alter cerebral artery contractility [J].
Bukoski, RD ;
Wang, SN ;
Bian, K ;
DeWitt, DS .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1997, 272 (03) :H1406-H1411
[9]   Extracellular release of serotonin following fluid-percussion brain injury in rats [J].
Busto, R ;
Dietrich, WD ;
Globus, MYT ;
Alonso, O ;
Ginsberg, MD .
JOURNAL OF NEUROTRAUMA, 1997, 14 (01) :35-42
[10]   Light and electron microscope study of nerve cells in traumatic oedematous human cerebral cortex [J].
Castejon, OJ ;
Valero, C ;
Diaz, M .
BRAIN INJURY, 1997, 11 (05) :363-388