Lactate administration attenuates cognitive deficits following traumatic brain injury

被引:102
作者
Rice, AC [1 ]
Zsoldos, R
Chen, T
Wilson, MS
Alessandri, B
Hamm, RJ
Bullock, MR
机构
[1] Virginia Commonwealth Univ, Med Coll Virginia, Dept Neurosurg, Richmond, VA 23298 USA
[2] Virginia Commonwealth Univ, Med Coll Virginia, Dept Psychol, Richmond, VA 23298 USA
关键词
Morris water maze; lateral fluid percussion injury;
D O I
10.1016/S0006-8993(01)03299-1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Moderately head injured patients often suffer long term neurological sequelae. There is no therapy for brain trauma and current treatments aim only to minimize secondary damage. These secondary effects we often triggered by the inability to re-establish ionic homeostasis after injury, due to large energy demands. Recent reports have demonstrated that neurons are capable of utilizing lactate as an energy source, thus this report examines the usefulness of lactate administration in the attenuation of behavioural deficits following a moderate brain injury. Lactate infusion (i.v.) was started 30 min after lateral fluid percussion injury and continued for 3 h. Cognitive deficits were determined using the Morris water maze. Lactate infused injured animals demonstrated significantly less cognitive deficits than saline infused injured animals. Thus, lactate infusion attenuated the cognitive deficits normally observed in this model, and therefore may provide moderately head injured patients with a treatment to help ameliorate the sequelae. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:156 / 159
页数:4
相关论文
共 23 条
[1]  
Alvarez-Maubecin V, 2000, J NEUROSCI, V20, P4091
[2]   Lactate/glucose dynamics after rat fluid percussion brain injury [J].
Chen, T ;
Qian, YZ ;
Di, X ;
Rice, A ;
Zhu, JP ;
Bullock, R .
JOURNAL OF NEUROTRAUMA, 2000, 17 (02) :135-142
[3]   Brain lactate uptake increases at the site of impact after traumatic brain injury [J].
Chen, T ;
Qian, YZ ;
Rice, A ;
Zhu, JP ;
Di, X ;
Bullock, R .
BRAIN RESEARCH, 2000, 861 (02) :281-287
[4]   Early neuropathologic effects of mild or moderate hypoxemia after controlled cortical impact injury in rats [J].
Clark, RSB ;
Kochanek, PM ;
Dixon, CE ;
Chen, MZ ;
Marion, DW ;
Heineman, S ;
DeKosky, ST ;
Graham, SH .
JOURNAL OF NEUROTRAUMA, 1997, 14 (04) :179-189
[5]   A FLUID PERCUSSION MODEL OF EXPERIMENTAL BRAIN INJURY IN THE RAT [J].
DIXON, CE ;
LYETH, BG ;
POVLISHOCK, JT ;
FINDLING, RL ;
HAMM, RJ ;
MARMAROU, A ;
YOUNG, HF ;
HAYES, RL .
JOURNAL OF NEUROSURGERY, 1987, 67 (01) :110-119
[6]   MILD EXPERIMENTAL BRAIN INJURY IN THE RAT INDUCES COGNITIVE DEFICITS ASSOCIATED WITH REGIONAL NEURONAL LOSS IN THE HIPPOCAMPUS [J].
HICKS, RR ;
SMITH, DH ;
LOWENSTEIN, DH ;
MARIE, RS ;
MCINTOSH, TK .
JOURNAL OF NEUROTRAUMA, 1993, 10 (04) :405-414
[7]  
Hilton G, 1994, Orthop Nurs, V13, P25, DOI 10.1097/00006416-199407000-00006
[8]   EFFECTS OF LACTATE AND PYRUVATE ON GLUCOSE DEPRIVATION IN RAT HIPPOCAMPAL SLICES [J].
IZUMI, Y ;
BENZ, AM ;
ZORUMSKI, CF ;
OLNEY, JW .
NEUROREPORT, 1994, 5 (05) :617-620
[9]   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
[10]  
Larrabee MG, 1996, J NEUROCHEM, V67, P1726