Lactate/glucose dynamics after rat fluid percussion brain injury

Tao Chen, Yong Zhen Qian, Xiao Di, Ann Rice, Jie Pei Zhu, Ross Bullock

Research output: Contribution to journalArticle

55 Citations (Scopus)

Abstract

Traumatic brain injury (TBI) places enormous early energy demand on brain tissue to reinstate normal ionic balance. Clinical studies have demonstrated a decline in extracellular fluid (ECF) glucose and an increase in lactate after TBI. In vitro studies suggest that this increase in lactate is mediated by increased glutamate and may provide a metabolic substrate for neurons, to aid in ionic restoration. This led us to hypothesize that high ECF lactate may be beneficial in recovery following TBI, where major ionic flux has been shown to occur. In this study, we measured cerebral dialysate lactate and glucose, and arterial lactate and glucose, before and after rat lateral fluid percussion brain injury (FPI; 2.06 ± 0.13 atm) with and without IV lactate infusion (100 mM X 0.65 mL/h X 5 h) to test the hypothesis that arterial lactate can influence ECF lactate. Dialysate lactate increased within 10 min following FPI, with higher values in the lactate infusion group. Following FPI, the dialysate lactate increase was 238% with lactate infusion versus 171% increase with saline infusion. Dialysate glucose fell immediately following FPI, with a more severe decline in the saline group. The glucose decrease was 231% greater in the IV saline group. Furthermore, in the lactate infusion group, the dialysate glucose levels recovered to baseline levels by 4 h after injury, whereas they remained depressed through out the experiment, in the saline infusion group. We conclude that arterial lactate augmentation can increase brain dialysate lactate, and result in more rapid recovery of dialysate glucose after FPI. This may indicate a beneficial role for lactate, that may be potentially useful in the clinical situation, after TBI.

Original languageEnglish
Pages (from-to)135-142
Number of pages8
JournalJournal of Neurotrauma
Volume17
Issue number2
StatePublished - Feb 1 2000
Externally publishedYes

Fingerprint

Percussion
Brain Injuries
Lactic Acid
Glucose
Dialysis Solutions
Extracellular Fluid
Brain

Keywords

  • Glucose
  • Lactate
  • Microdialysate
  • Traumatic brain injury

ASJC Scopus subject areas

  • Clinical Neurology
  • Neuroscience(all)

Cite this

Chen, T., Qian, Y. Z., Di, X., Rice, A., Zhu, J. P., & Bullock, R. (2000). Lactate/glucose dynamics after rat fluid percussion brain injury. Journal of Neurotrauma, 17(2), 135-142.

Lactate/glucose dynamics after rat fluid percussion brain injury. / Chen, Tao; Qian, Yong Zhen; Di, Xiao; Rice, Ann; Zhu, Jie Pei; Bullock, Ross.

In: Journal of Neurotrauma, Vol. 17, No. 2, 01.02.2000, p. 135-142.

Research output: Contribution to journalArticle

Chen, T, Qian, YZ, Di, X, Rice, A, Zhu, JP & Bullock, R 2000, 'Lactate/glucose dynamics after rat fluid percussion brain injury', Journal of Neurotrauma, vol. 17, no. 2, pp. 135-142.
Chen T, Qian YZ, Di X, Rice A, Zhu JP, Bullock R. Lactate/glucose dynamics after rat fluid percussion brain injury. Journal of Neurotrauma. 2000 Feb 1;17(2):135-142.
Chen, Tao ; Qian, Yong Zhen ; Di, Xiao ; Rice, Ann ; Zhu, Jie Pei ; Bullock, Ross. / Lactate/glucose dynamics after rat fluid percussion brain injury. In: Journal of Neurotrauma. 2000 ; Vol. 17, No. 2. pp. 135-142.
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