Institut National de la Santé et de la Recherche Médicale, Grenoble, France; Université Grenoble Alpes, Grenoble Institut des Neurosciences, Grenoble, France; Pôle Couple Enfant, Hôpital Michallon, CHU Grenoble Alpes, Grenoble, France.
Institut National de la Santé et de la Recherche Médicale, Grenoble, France; Université Grenoble Alpes, Grenoble Institut des Neurosciences, Grenoble, France; Pôle Anesthésie Réanimation, Hôpital Michallon, CHU Grenoble Alpes, Grenoble, France.
Br J Anaesth. 2018 Jun;120(6):1295-1303. doi: 10.1016/j.bja.2018.01.025. Epub 2018 Mar 20.
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).
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 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).
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 < 0.05], higher mitochondrial respiratory control ratio, higher tissue oxygen saturation [77% (71-79) vs 66% (55-73); P < 0.05], and reduced mitochondrial cristae thickness in astrocytes [27.5 (22.5-38.4) nm vs 38.4 (31.0-47.5) nm; P < 0.01] compared with the TBI-saline group. Serum sodium and lactate concentrations and serum osmolality were higher in the TBI-HSL than in the TBI-saline group.
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.
高渗乳酸钠（HSL）溶液在受损大脑中的作用机制尚不清楚。我们在弥漫性创伤性脑损伤（TBI）的啮齿动物模型中研究了 HSL 对大脑代谢、氧合和灌注的影响。
创伤后 30 分钟，麻醉成年大鼠随机分为接受生理盐水（TBI-盐水组）或 HSL（TBI-HSL 组）3 小时输注。假手术-盐水组和假手术-HSL 组未受损伤。在 TBI（或等效物）后进行了三组实验，以研究：1）使用扩散加权磁共振成像研究脑水肿，使用局部 H-磁共振波谱研究脑代谢（每组 10 只大鼠）。然后使用提取的线粒体的测氧仪分析确定呼吸控制比，2）使用定量血氧水平依赖性磁共振方法研究脑氧合和灌注（每组 10 只大鼠），以及 3）线粒体超微结构变化（每组 1 只大鼠）。
与 TBI-盐水组相比，TBI-HSL 组和假手术组脑水肿减少。同时，TBI-HSL 组细胞内乳酸/肌酸比值较低[0.049（0.047-0.098）比 0.097（0.079-0.157）；P<0.05]，线粒体呼吸控制比更高，组织氧饱和度更高[77%（71-79）比 66%（55-73）；P<0.05]，星形胶质细胞中线粒体嵴厚度降低[27.5（22.5-38.4）nm 比 38.4（31.0-47.5）nm；P<0.01]与 TBI-盐水组相比。TBI-HSL 组血清钠和乳酸浓度以及血清渗透压高于 TBI-盐水组。
这些发现表明，高渗乳酸钠溶液可通过血管扩张、线粒体和抗水肿作用逆转创伤性脑损伤后的脑氧合和代谢功能障碍。
