A Comparison of Oxidative Lactate Metabolism in Traumatically Injured Brain and Control Brain.

Abstract

Metabolic abnormalities occur after traumatic brain injury (TBI). Glucose is conventionally regarded as the major energy substrate, although lactate can also be an energy source. We compared 3-13C lactate metabolism in TBI with “normal” control brain and muscle, measuring 13C-glutamine enrichment to assess tricarboxylic acid (TCA) cycle metabolism. Microdialysis catheters in 9 severe TBI patients’ brains, 5 non-TBI brain surgical patients, and 5 resting muscle (non-TBI) patients were perfused (24h in brain, 8h in muscle) with 8 mmol/L sodium 3 13C lactate. Microdialysate analysis employed ISCUS and NMR. In TBI, with 3-13C lactate perfusion, microdialysate glucose concentration increased non-significantly (mean +11.9%, p=0.463), with significant increases (p=0.028) for lactate (+174%), pyruvate (+35.8%), and lactate/pyruvate ratio (+101.8%). Microdialysate 13C-glutamine fractional enrichments (median, IQR) were: for C4 5.1(0–11.1)% in TBI and 5.7(4.6–6.8)% in control brain, for C3 0(0–5.0)% in TBI and 0(0-0) % in control brain, and for C2 2.9(0–5.7)% in TBI and 1.8(0–3.4)% in control brain. 13C-enrichments were not statistically different between TBI and control brain, showing both metabolise 3-13C lactate via TCA cycle, in contrast to muscle. Several TBI patients exhibited 13C-glutamine enrichment above the non-TBI control range, suggesting lactate oxidative metabolism as a TBI “emergency option”.