LACTATE ACCUMULATION FOLLOWING CONCUSSIVE BRAIN INJURY - THE ROLE OF IONIC FLUXES INDUCED BY EXCITATORY AMINO-ACIDS

被引:157
作者
KAWAMATA, T
KATAYAMA, Y
HOVDA, DA
YOSHINO, A
BECKER, DP
机构
[1] Division of Neurosurgery, UCLA School of Medicine, Los Angeles, CA 90024-6901
关键词
CONCUSSION; IONIC FLUX; LACTATE; EXCITATORY AMINO ACID; GLUCOSE METABOLISM; MICRODIALYSIS; GLYCOLYSIS;
D O I
10.1016/0006-8993(94)01444-M
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
During the first few minutes following traumatic brain injury, cells are exposed to an indiscriminate release of glutamate from nerve terminals resulting in a massive tonic flux (e.g., K+ efflux) via stimulation of excitatory amino acid (EAA)-coupled ion channels. The present study was undertaken to elucidate the causal relationship between these ionic shifts and lactate accumulation in the injured brain, by examining the effects of ouabain (an inhibitor of Na+/K+-ATPase), Ba2+ (an inhibitor of non-energy-dependent glial K+ uptake) and kynurenic acid (KYN; a broad-spectrum EAA antagonist) on lactate accumulation. Two microdialysis probes were placed bilaterally in the rat parietal cortex. One was perfused with a test drug (1.0 mM ouabain, 2.0 mM Ba2+ or 10 mM KYN) and the other with Ringer's solution (control) for 30 min prior to injury. Following a 2.2-2.7 atm fluid-percussion injury, lactate levels in the dialysate increased (up to 116.6% above baseline) for the first 16 min and returned to baseline levels within 20 min after injury. This lactate accumulation was attenuated by preinjury administration of ouabain and KYN and was prolonged by Ba2+ administration. These findings indicate that lactate accumulation following concussive brain injury is a result of increased glycolysis which supports ion-pumping mechanisms, thereby, restoring the ionic balance which was disrupted by stimulation of EAA-coupled ion channels.
引用
收藏
页码:196 / 204
页数:9
相关论文
共 62 条
[1]   GLYCOLYSIS-INDUCED DISCORDANCE BETWEEN GLUCOSE METABOLIC RATES MEASURED WITH RADIOLABELED FLUORODEOXYGLUCOSE AND GLUCOSE [J].
ACKERMANN, RF ;
LEAR, JL .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1989, 9 (06) :774-785
[2]   THE EFFECTS OF TRANSMITTERS ON THE AFFINITY OF THE INSOLUBLE FRACTION OF OX BRAIN FOR NA+ AND K+ [J].
AHMED, N ;
HILLMAN, H .
NEUROCHEMICAL RESEARCH, 1989, 14 (02) :179-184
[3]  
ALBERS RW, 1989, BASIC NEUROCHEMISTRY, P52
[4]  
AMES A, 1992, J NEUROSCI, V12, P4234
[5]  
ANDERSEN BJ, 1989, INTRACRANIAL PRESSUR, V7, P575
[6]   ENERGY-REQUIRING CELL FUNCTIONS IN THE ISCHEMIC BRAIN - THEIR CRITICAL SUPPLY AND POSSIBLE INHIBITION IN PROTECTIVE THERAPY [J].
ASTRUP, J .
JOURNAL OF NEUROSURGERY, 1982, 56 (04) :482-497
[7]  
ASTRUP J, 1981, STROKE, V726, P730
[8]   ION ACTIVITIES AND POTASSIUM UPTAKE MECHANISMS OF GLIAL-CELLS IN GUINEA-PIG OLFACTORY CORTEX SLICES [J].
BALLANYI, K ;
GRAFE, P ;
TENBRUGGENCATE, G .
JOURNAL OF PHYSIOLOGY-LONDON, 1987, 382 :159-174
[9]  
DESALLES A A F, 1986, Society for Neuroscience Abstracts, V12, P967
[10]   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