Real time monitoring of glutamate following fluid percussion brain injury with hypoxia in the rat

被引:0
作者
Matsushita, Y [1 ]
Shima, K [1 ]
Nawashiro, H [1 ]
Wada, K [1 ]
Tsuzuki, N [1 ]
Miyazawa, T [1 ]
机构
[1] Natl Def Med Coll, Dept Neurosurg, Tokorozawa, Saitama 3598513, Japan
来源
BRAIN EDEMA XI | 2000年 / 76卷
关键词
apoptosis; biosensor; glutamate; lateral fluid-percussion;
D O I
暂无
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
In this study, extracellular glutamate (Glu) was monitored in real time using a biosensor following traumatic brain injury (TBI) either with or without inducing hypoxia in the rat Fluid-percussion model. We also measured the cortical contusion volume at 3 days after the insult. The animals were divided into 3 groups. Group I was subjected to TBI only, Group 2 to TBI followed by 20 min of moderate hypoxia (FiO2: 10%) and Group 3 to 20 min of moderate hypoxia without TBI. The surge increase in the extracellular Glu concentration occurred immediately after TBI in Groups I and 2. Group 2 showed a prolonged efflux of Glu during hypoxia. Group 3 Glu showed low continuous steady levels. The contusion volume in Group 2 was significantly larger than in Group 1. To test the possible involvement of apoptosis in Groups I and 2, rats were sacrificed at 1, 6, 24 and 72 h after TBI. Immunohistochemical studies showed an increased number of both CPP32 positive cells at 24 h and TUNEL cells at 72 h in Group 2. These results suggest that TBI with moderate hypoxia induced a prolonged efflux of Glu that resulted more cortical damage due to necrosis and apoptosis.
引用
收藏
页码:207 / 212
页数:6
相关论文
共 33 条
  • [1] Real time monitoring of biphasic glutamate release using dialysis electrode in rat acute brain ischemia
    Asai, S
    Iribe, Y
    Kohno, T
    Ishikawa, K
    [J]. NEUROREPORT, 1996, 7 (05) : 1092 - 1096
  • [2] THE ROLE OF SECONDARY BRAIN INJURY IN DETERMINING OUTCOME FROM SEVERE HEAD-INJURY
    CHESNUT, RM
    MARSHALL, LF
    KLAUBER, MR
    BLUNT, BA
    BALDWIN, N
    EISENBERG, HM
    JANE, JA
    MARMAROU, A
    FOULKES, MA
    [J]. JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE, 1993, 34 (02) : 216 - 222
  • [3] CHESNUT RM, 1993, ACTA NEUROCHIR, P121
  • [4] Early neuropathologic effects of mild or moderate hypoxemia after controlled cortical impact injury in rats
    Clark, RSB
    Kochanek, PM
    Dixon, CE
    Chen, MZ
    Marion, DW
    Heineman, S
    DeKosky, ST
    Graham, SH
    [J]. JOURNAL OF NEUROTRAUMA, 1997, 14 (04) : 179 - 189
  • [5] Conti AC, 1998, J NEUROSCI, V18, P5663
  • [6] Hypoxia potentiates traumatic brain injury-induced expression of c-fos in rats
    Dave, JR
    Bauman, RA
    Long, JB
    [J]. NEUROREPORT, 1997, 8 (02) : 395 - 398
  • [7] Delayed posttraumatic brain hyperthermia worsens outcome after fluid percussion brain injury: A light and electron microscopic study in rats
    Dietrich, WD
    Alonso, O
    Halley, M
    Busto, R
    [J]. NEUROSURGERY, 1996, 38 (03) : 533 - 541
  • [8] EARLY MICROVASCULAR AND NEURONAL CONSEQUENCES OF TRAUMATIC BRAIN INJURY - A LIGHT AND ELECTRON-MICROSCOPIC STUDY IN RATS
    DIETRICH, WD
    ALONSO, O
    HALLEY, M
    [J]. JOURNAL OF NEUROTRAUMA, 1994, 11 (03) : 289 - 301
  • [9] IDENTIFICATION OF PROGRAMMED CELL-DEATH INSITU VIA SPECIFIC LABELING OF NUCLEAR-DNA FRAGMENTATION
    GAVRIELI, Y
    SHERMAN, Y
    BENSASSON, SA
    [J]. JOURNAL OF CELL BIOLOGY, 1992, 119 (03) : 493 - 501
  • [10] ISCHEMIC BRAIN-DAMAGE IS STILL COMMON IN FATAL NON-MISSILE HEAD-INJURY
    GRAHAM, DI
    FORD, I
    ADAMS, JH
    DOYLE, D
    TEASDALE, GM
    LAWRENCE, AE
    MCLELLAN, DR
    [J]. JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY, 1989, 52 (03) : 346 - 350