Lactate supplementation in severe traumatic brain injured adults by primed constant infusion of sodium L-lactate.
Level 4 - case-series / case-control
Uncontrolled single-arm interventional physiological study
PubMed 28543565 · doi:10.1002/jnr.24085
What was done
Researchers administered a primed constant sodium L-lactate infusion to 11 adult neurocritical care patients with moderate-to-severe traumatic brain injury. Blood samples were collected before and periodically during the infusion to measure systemic metabolites and calculate the arteriovenous difference of lactate (AVDlac) and glucose to quantify global cerebral uptake.
What was found
Sodium L-lactate infusion converted net cerebral lactate release into net cerebral lactate uptake. Based on a mixed-effects model, doubling arterial lactate concentration from 0.92 to 1.84 mM shifted AVDlac from -0.078 mM to 0.090 mM. Systemic glucose levels did not change significantly, while significant increases from baseline occurred for alanine (30% [20 to 39]), glutamine (34% [24 to 43]), acetate (87% [60 to 113]), valine (40% [28 to 51]), and leucine (24% [16 to 32]).
Why it matters
This study provides preliminary human physiological evidence that exogenous lactate supplementation can switch the injured brain from net lactate excretion to net lactate consumption, supporting its potential role as an alternative cerebral fuel substrate.
Limits
The study is limited by a very small sample size (n = 11) and the absence of a control or placebo group. It evaluated only acute biochemical and metabolic indices; clinical endpoints, neurological recovery, and overall safety outcomes were not evaluated.
Cited by
- supports Infusing lactate in patients with traumatic brain injury increases total cerebral carbohydrate uptake (glucose plus lactate).