Hypertonic sodium lactate reverses brain oxygenation and metabolism dysfunction after traumatic brain injury

Background The mechanisms by which hypertonic sodium lactate (HSL) solution act in injured brain are unclear. We investigated the effects of HSL on brain metabolism, oxygenation, and perfusion in a rodent model of diffuse traumatic brain injury (TBI). Methods Thirty minutes after trauma, anaesthetised adult rats were randomly assigned to receive a 3 h infusion of either a saline solution (TBI–saline group) or HSL (TBI–HSL group). The sham–saline and sham–HSL groups received no insult. Three series of experiments were conducted up to 4 h after TBI (or equivalent) to investigate: 1) brain oedema using diffusion-weighted magnetic resonance imaging and brain metabolism using localized 1 H-magnetic resonance spectroscopy ( n = 10 rats per group). The respiratory control ratio was then determined using oxygraphic analysis of extracted mitochondria, 2) brain oxygenation and perfusion using quantitative blood-oxygenation-level-dependent magnetic resonance approach ( n = 10 rats per group), and 3) mitochondrial ultrastructural changes ( n = 1 rat per group). Results Compared with the TBI–saline group, the TBI–HSL and the sham-operated groups had reduced brain oedema. Concomitantly, the TBI–HSL group had lower intracellular lactate/creatine ratio [0.049 (0.047–0.098) vs 0.097 (0.079–0.157); P vs 66% (55–73); P vs 38.4 (31.0–47.5) nm; P Conclusions These findings indicate that the hypertonic sodium lactate solution can reverse brain oxygenation and metabolism dysfunction after traumatic brain injury through vasodilatory, mitochondrial, and anti-oedema effects.