Changes in Brain Tissue Oxygenation After Treatment of Diffuse Traumatic Brain Injury by Erythropoietin
Changes in Brain Tissue Oxygenation After Treatment of Diffuse Traumatic Brain Injury by Erythropoietin
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DOI：
10.1097/ccm.0b013e31827ca64e
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发表时间：
2013-05-01
影响因子：
8.8
通讯作者：
Payen, Jean-Francois
中科院分区：
文献类型：
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作者：
Bouzat, Pierre;Millet, Anne;Payen, Jean-Francois
目的：研究重组人促红细胞生成素对弥漫性创伤性脑损伤模型中脑氧合的影响。设计：成年雄性 Wistar 大鼠。环境：神经科学和生理学实验室。干预：弥漫性创伤性脑损伤（冲击加速模型）后 30 分钟，给大鼠静脉注射生理盐水或重组人促红细胞生成素（5000 IU/kg）。第三组未接受创伤性脑损伤损伤（假手术）。测量和主要结果：在创伤性脑损伤后 2 小时进行了三个系列的实验，以研究：1）使用扩散加权磁共振成像和表观扩散系数测量重组人促红细胞生成素对脑水肿的影响（每组 n = 11 只大鼠）；随后使用基于多参数磁共振的方法测量局部脑氧饱和度、平均通过时间和血容量分数，以估计新皮质和尾壳核的脑氧合和脑灌注； 2）类似实验中重组人促红细胞生成素对脑组织PO2的影响（每组n=5只大鼠）； 3）治疗后皮质超微结构的变化（每组n = 1只大鼠）。与假手术组相比，创伤性脑损伤盐水组大鼠局部脑氧饱和度和脑组织 PO2 显着降低，同时出现脑水肿形成和微血管管腔塌陷。重组人促红细胞生成素治疗逆转了所有这些创伤性脑损伤引起的变化。三组动物的脑灌注（平均通过时间和血容量分数）相当。结论：我们的研究结果表明，脑缺氧可能与微循环紊乱和细胞水肿有关，但没有脑缺血的证据。这些变化通过创伤后施用重组人促红细胞生成素得以逆转，从而为该药物在脑损伤中的应用提供了新的视角。 （《重症监护医学》2013 年；41：1316-1324）
Objectives: To investigate the effects of recombinant human erythropoietin on brain oxygenation in a model of diffuse traumatic brain injury.Design: Adult male Wistar rats.Setting: Neurosciences and physiology laboratories.Interventions: Thirty minutes after diffuse traumatic brain injury (impact-acceleration model), rats were intravenously administered with either a saline solution or a recombinant human erythropoietin (5000 IU/kg). A third group received no traumatic brain injury insult (sham-operated).Measurements and Main Results: Three series of experiments were conducted 2 hours after traumatic brain injury to investigate: 1) the effect of recombinant human erythropoietin on brain edema using diffusion-weighted magnetic resonance imaging and measurements of apparent diffusion coefficient (n = 11 rats per group); local brain oxygen saturation, mean transit time, and blood volume fraction were subsequently measured using a multiparametric magnetic resonance-based approach to estimate brain oxygenation and brain perfusion in the neocortex and caudoputamen; 2) the effect of recombinant human erythropoietin on brain tissue PO2 in similar experiments (n = 5 rats per group); and 3) the cortical ultrastructural changes after treatment (n = 1 rat per group). Compared with the sham-operated group, traumatic brain injury saline rats showed a significant decrease in local brain oxygen saturation and in brain tissue PO2 alongside brain edema formation and microvascular lumen collapse at H2. Treatment with recombinant human erythropoietin reversed all of these traumatic brain injury-induced changes. Brain perfusion (mean transit time and blood volume fraction) was comparable between the three groups of animals.Conclusion: Our findings indicate that brain hypoxia can be related to microcirculatory derangements and cell edema without evidence of brain ischemia. These changes were reversed with post-traumatic administration of recombinant human erythropoietin, thus offering new perspectives in the use of this drug in brain injury. (Crit Care Med 2013; 41:1316-1324)