Time course of changes in lactate and free fatty acids after experimental brain injury and relationship to morphologic damage

被引:73
作者
Dhillon, HS [1 ]
Dose, JM [1 ]
Scheff, SW [1 ]
Prasad, MR [1 ]
机构
[1] UNIV KENTUCKY, ALBERT B CHANDLER MED CTR, DEPT ANAT & NEUROBIOL, LEXINGTON, KY 40536 USA
关键词
D O I
10.1006/exnr.1997.6524
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
Regional levels of lactate and free fatty acids (FFA) were measured after lateral fluid percussion (FP) brain injury in rats. At 5 min after injury, tissue concentrations of lactate were elevated in the cortices and hippocampi of both ipsilateral and contralateral hemispheres. Whereas lactate levels had returned to normal by about 20 min after injury in the penumbra and contralateral cortices, their elevation persisted in the ipsilateral injured cortex and hippocampus for 24 h after injury. Increases in the levels of FFA (particularly stearic and arachidonic acids) were observed in the cortices and hippocampi of both ipsilateral and contralateral hemispheres at 5 min after injury; these levels returned to normal in only the penumbra and contralateral cortices by 20 min after injury. Increased amounts of palmitic and oleic acids were also found only in the injured left cortex and ipsilateral hippocampus at 20 min or later after injury. In general, these elevations persisted for as long as 6 to 24 h in the injured cortex and for 2.5 to 24 h after injury in the ipsilateral hippocampus. Histologic studies revealed a similar extent of damage in the cortex between 5 min and 24 h after injury, whereas damage in the CA3 region of the ipsilateral hippocampus increased during that period. These findings suggest a role for lactic acid and FFA, two secondary injury factors, in neuronal cell loss after brain injury. (C) 1997 Academic Press.
引用
收藏
页码:240 / 249
页数:10
相关论文
共 62 条
[21]
HAYES RL, 1992, J NEUROTRAUM, V9, pS173
[22]
Temporal and spatial characterization of neuronal injury following lateral fluid-percussion brain injury in the rat [J].
Hicks, R ;
Soares, H ;
Smith, D ;
McIntosh, T .
ACTA NEUROPATHOLOGICA, 1996, 91 (03) :236-246
[23]
TEMPORAL RESPONSE AND EFFECTS OF EXCITATORY AMINO-ACID ANTAGONISM ON MICROTUBULE-ASSOCIATED PROTEIN-2 IMMUNOREACTIVITY FOLLOWING EXPERIMENTAL BRAIN INJURY IN RATS [J].
HICKS, RR ;
SMITH, DH ;
MCINTOSH, TK .
BRAIN RESEARCH, 1995, 678 (1-2) :151-160
[24]
HOVDA DA, 1992, J NEUROTRAUM, V9, pS47
[25]
DIFFUSE PROLONGED DEPRESSION OF CEREBRAL OXIDATIVE-METABOLISM FOLLOWING CONCUSSIVE BRAIN INJURY IN THE RAT - A CYTOCHROME-OXIDASE HISTOCHEMISTRY STUDY [J].
HOVDA, DA ;
YOSHINO, A ;
KAWAMATA, T ;
KATAYAMA, Y ;
BECKER, DP .
BRAIN RESEARCH, 1991, 567 (01) :1-10
[26]
PRODUCTION AND CLEARANCE OF LACTATE FROM BRAIN-TISSUE, CEREBROSPINAL-FLUID, AND SERUM FOLLOWING EXPERIMENTAL BRAIN INJURY [J].
INAO, S ;
MARMAROU, A ;
CLARKE, GD ;
ANDERSEN, BJ ;
FATOUROS, PP ;
YOUNG, HF .
JOURNAL OF NEUROSURGERY, 1988, 69 (05) :736-744
[27]
THE EFFECTS OF HYPOVOLEMIC HYPOTENSION ON HIGH-ENERGY PHOSPHATE-METABOLISM OF TRAUMATIZED BRAIN IN RATS [J].
ISHIGE, N ;
PITTS, LH ;
BERRY, I ;
NISHIMURA, MC ;
JAMES, TL .
JOURNAL OF NEUROSURGERY, 1988, 68 (01) :129-136
[28]
MASSIVE INCREASES IN EXTRACELLULAR POTASSIUM AND THE INDISCRIMINATE RELEASE OF GLUTAMATE FOLLOWING CONCUSSIVE BRAIN INJURY [J].
KATAYAMA, Y ;
BECKER, DP ;
TAMURA, T ;
HOVDA, DA .
JOURNAL OF NEUROSURGERY, 1990, 73 (06) :889-900
[29]
LACTATE ACCUMULATION FOLLOWING CONCUSSIVE BRAIN INJURY - THE ROLE OF IONIC FLUXES INDUCED BY EXCITATORY AMINO-ACIDS [J].
KAWAMATA, T ;
KATAYAMA, Y ;
HOVDA, DA ;
YOSHINO, A ;
BECKER, DP .
BRAIN RESEARCH, 1995, 674 (02) :196-204
[30]
APPEARANCE OF SUPEROXIDE ANION RADICAL IN CEREBRAL EXTRACELLULAR-SPACE DURING INCREASED PROSTAGLANDIN SYNTHESIS IN CATS [J].
KONTOS, HA ;
WEI, EP ;
ELLIS, EF ;
JENKINS, LW ;
POVLISHOCK, JT ;
ROWE, GT ;
HESS, ML .
CIRCULATION RESEARCH, 1985, 57 (01) :142-151