Department of Intensive Care Medicine, Neuroscience Critical Care Research Group, Faculty of Biology and Medicine, University Hospital of Lausanne, Rue du Bugnon 46, 1011, Lausanne, Switzerland,
Intensive Care Med. 2014 Mar;40(3):412-21. doi: 10.1007/s00134-013-3203-6. Epub 2014 Jan 30.
Experimental evidence suggests that lactate is neuroprotective after acute brain injury; however, data in humans are lacking. We examined whether exogenous lactate supplementation improves cerebral energy metabolism in humans with traumatic brain injury (TBI).
We prospectively studied 15 consecutive patients with severe TBI monitored with cerebral microdialysis (CMD), brain tissue PO2 (PbtO2), and intracranial pressure (ICP). Intervention consisted of a 3-h intravenous infusion of hypertonic sodium lactate (aiming to increase systemic lactate to ca. 5 mmol/L), administered in the early phase following TBI. We examined the effect of sodium lactate on neurochemistry (CMD lactate, pyruvate, glucose, and glutamate), PbtO2, and ICP.
Treatment was started on average 33 ± 16 h after TBI. A mixed-effects multilevel regression model revealed that sodium lactate therapy was associated with a significant increase in CMD concentrations of lactate [coefficient 0.47 mmol/L, 95% confidence interval (CI) 0.31-0.63 mmol/L], pyruvate [13.1 (8.78-17.4) μmol/L], and glucose [0.1 (0.04-0.16) mmol/L; all p < 0.01]. A concomitant reduction of CMD glutamate [-0.95 (-1.94 to 0.06) mmol/L, p = 0.06] and ICP [-0.86 (-1.47 to -0.24) mmHg, p < 0.01] was also observed.
Exogenous supplemental lactate can be utilized aerobically as a preferential energy substrate by the injured human brain, with sparing of cerebral glucose. Increased availability of cerebral extracellular pyruvate and glucose, coupled with a reduction of brain glutamate and ICP, suggests that hypertonic lactate therapy has beneficial cerebral metabolic and hemodynamic effects after TBI.
实验证据表明，乳酸在急性脑损伤后具有神经保护作用；然而，人类的数据尚缺乏。我们研究了外源性乳酸补充是否能改善创伤性脑损伤（TBI）患者的大脑能量代谢。
我们前瞻性地研究了 15 例连续的 TBI 患者，这些患者通过脑微透析（CMD）、脑组织氧分压（PbtO2）和颅内压（ICP）进行监测。干预措施包括在 TBI 后早期进行 3 小时的高渗乳酸钠静脉输注（旨在将全身乳酸增加到约 5mmol/L）。我们研究了乳酸钠对神经化学（CMD 中的乳酸、丙酮酸、葡萄糖和谷氨酸）、PbtO2 和 ICP 的影响。
治疗开始于 TBI 后平均 33±16 小时。混合效应多级回归模型显示，乳酸钠治疗与 CMD 中乳酸浓度的显著增加相关[0.47mmol/L，95%置信区间（CI）0.31-0.63mmol/L]，丙酮酸增加[13.1（8.78-17.4）μmol/L]，葡萄糖增加[0.1（0.04-0.16）mmol/L；所有 p<0.01]。同时观察到 CMD 谷氨酸减少[-0.95（-1.94 至 0.06）mmol/L，p=0.06]和 ICP 减少[-0.86（-1.47 至-0.24）mmHg，p<0.01]。
外源性补充的乳酸可以被受损的人脑有氧利用作为一种优先的能量底物，同时节省脑葡萄糖。脑细胞外丙酮酸和葡萄糖的可用性增加，加上脑谷氨酸和 ICP 的减少，表明高渗乳酸治疗在 TBI 后具有有益的脑代谢和血液动力学效应。
