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 language | English |
|---|---|
| Pages (from-to) | 135-142 |
| Number of pages | 8 |
| Journal | Journal of Neurotrauma |
| Volume | 17 |
| Issue number | 2 |
| State | Published - Feb 1 2000 |
| Externally published | Yes |
Fingerprint
Keywords
- Glucose
- Lactate
- Microdialysate
- Traumatic brain injury
ASJC Scopus subject areas
- Clinical Neurology
- Neuroscience(all)
Cite this
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 journal › Article
}
TY - JOUR
T1 - Lactate/glucose dynamics after rat fluid percussion brain injury
AU - Chen, Tao
AU - Qian, Yong Zhen
AU - Di, Xiao
AU - Rice, Ann
AU - Zhu, Jie Pei
AU - Bullock, Ross
PY - 2000/2/1
Y1 - 2000/2/1
N2 - 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.
AB - 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.
KW - Glucose
KW - Lactate
KW - Microdialysate
KW - Traumatic brain injury
UR - http://www.scopus.com/inward/record.url?scp=0033994101&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0033994101&partnerID=8YFLogxK
M3 - Article
C2 - 10709871
AN - SCOPUS:0033994101
VL - 17
SP - 135
EP - 142
JO - Journal of Neurotrauma
JF - Journal of Neurotrauma
SN - 0897-7151
IS - 2
ER -