高渗乳酸对急性脑损伤后脑灌注及葡萄糖利用率的影响
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Hypertonic Lactate to Improve Cerebral Perfusion
and Glucose Availability After Acute Brain Injury*
背景与目的
乳酸可促进脑血流，在葡萄糖缺乏时，其是脑代谢的有效替代底物之一。高渗乳酸已被证明在实验性脑损伤模型中具有神经保护的作用，但这一作用尚未在人体得到求证。
方 法
本试验为前瞻性研究， 23例脑损伤受试者（13例脑外伤，10例蛛网膜下腔出血；平均年龄59岁；格拉斯哥昏迷量表评分平均为6 [3-7]）。所有入组患者受伤后平均39h（26-49h）内予以高渗乳酸液静脉输注3h（乳酸钠，1000mmol/ L;浓度，30mol/kg-1/min-1）。应用经颅多普勒（TCD，经颞部）评估高渗性乳酸对脑灌注的影响，在输注高渗乳酸液前监测颅内压（ICP）作为基线值。在输注高渗乳酸液的3h期间，应用脑微渗析探针每60 min检测脑能量代谢，检测乳酸、丙酮酸和糖的浓度水平；同时监测患者的颅内灌注压（CCP）和脑组织氧合（Pbto2）。
结 果
尽管所有患者的颅内压基线正常，但是大多数受试者（13/23 = 57％）的脑葡萄糖利用率降低（基线葡萄糖，<1 mmol / L）。输注高渗乳酸液后，患者脑代谢乳酸增加（+ 55％[31-80％]），葡萄糖升高超过正常范围（+ 42％[30%-78％]; P <0.05）;脑葡萄糖利用率降低与脑内可用葡萄糖增加明显相关（r = -0.53; P= 0.009，）。此外，患者颅内压在治疗期间明显下降，而ICP、MAP、Pbto2和PaCO2没有明显改变。与颅脑外伤患者相比，蛛网膜下腔出血患者CBFV下降似更明显，但无统计学意义。
结 论
高渗乳酸能改善成人脑损伤后的脑灌注压和脑葡萄糖利用量，但这种作用可能与脑乳酸的增加有关，而不是与全身反应有关。
原始文献摘要
Carteron L, Solari D, Patet C, et al. Hypertonic Lactate to Improve Cerebral Perfusion and Glucose Availability After Acute Brain Injury.[J]. Critical Care Medicine, 2018, online first:1.
Objectives: Lactate promotes cerebral blood flow and is an efficient substrate for the brain, particularly at times of glucose shortage.Hypertonic lactate is neuroprotective after experimental brain injury; however, human data are limited.
Design: Prospective study (clinicaltrials.gov NCT01573507).
Setting: Academic ICU. Patients: Twenty-three brain-injured subjects (13 traumatic brain injury/10 subarachnoid hemorrhage; median age, 59 yr [41–65 yr]; median Glasgow Coma Scale, 6 [3–7]).
Interventions: Three-hour IV infusion of hypertonic lactate (sodium lactate, 1,000 mmol/L; concentration, 30 μmol/kg/min) administered 39 hours (26–49 hr) from injury.
Measurements and Main Results: We examined the effect of hypertonic lactate on cerebral perfusion (using transcranial Doppler) and brain energy metabolism (using cerebral microdialysis). The majority of subjects (13/23 = 57%) had reduced brain glucose availability (baseline pretreatment cerebral microdialysis glucose, < 1 mmol/L) despite normal baseline intracranial pressure (10 [7–15] mm Hg). Hypertonic lactate was associated with increased cerebral microdialysis lactate (+55% [31–80%]) that was paralleled by an increase in middle cerebral artery mean cerebral
blood flow velocities (+36% [21–66%]) and a decrease in pulsatility index (–21% [13–26%]; all p < 0.001). Cerebral microdialysis glucose increased above normal range during hypertonic lactate (+42% [30–78%]; p < 0.05); reduced brain glucose availability correlated with a greater improvement of cerebral microdialysis glucose (Spearman r = –0.53; p = 0.009). No significant changes in cerebral perfusion pressure, mean arterial pressure, systemic carbon dioxide, and blood glucose were observed during hypertonic lactate (all p > 0.1).
Conclusions: This is the first clinical demonstration that hypertonic lactate resuscitation improves both cerebral perfusion and brain glucose availability after brain injury. These cerebral vascular and metabolic effects appeared related to brain lactate supplementation rather than to systemic effects.
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贵州医科大学高鸿教授课题组
编辑：余晓旭 审校：王贵龙