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在创伤性出血损伤后的心肌变化

Rebecca Simpson¹, Banjerd Praditsuktavorn, Johanna Wall

¹From the Centre for Trauma Sciences, Blizard Institute (R.S., B.P., J.W., C.T., J.L.T., K.B.), Metabolomics Core Facility, Barts Cancer Institute (V.M.), Centre for Translational Medicine and Therapeutics, William Harvey Research Institute (C.T.), Barts and the London School of Medicine and Dentistry, Queen Mary University, London, United Kingdom.

The journal of trauma and acute care surgery

|May 30, 2023

概括

创伤性出血性休克会通过氧化应激和新陈代谢变化引起心脏功能障碍. 这项研究确定了关键的代谢变化,为新的心脏保护疗法提供了潜在的目标,以减少创伤死亡率.

科学领域:

心血管研究研究心血管研究
创伤医学创伤医学
代谢学代谢学代谢学

背景情况:

心脏功能障碍 (CD) 是创伤后器官衰竭和死亡的主要原因.
创伤后炎症与CD联系的确切途径尚未完全理解.
目前对创伤引起的CD缺乏治疗方法.

研究的目的:

为了调查心肌氧化应激在创伤性出血损伤后CD中的作用.
为了确定心肌中相关的代谢概况变化.

主要方法:

从压力控制创伤出血休克 (THS) 的小鼠模型中分析出活体心脏组织.
免疫组织化学用于评估氧化应激标志物8-基-2'-脱氧氨酸.
液体染色学-质谱学 (LC-MS) 进行了代谢分析.

主要成果:

与对照组相比,THS损伤显著增加了心肌8-基-2'-脱氧氨的表达.
创伤性出血性休克导致氨酸增加,心肌中的酸盐和谷氨酸盐水平降低.
这些变化表明了催化代谢和氧化应激的激活.

结论:

急性氧化应激和心脏能量代谢的改变发生在创伤性出血后.
这些发现提供了关于炎症,心脏收缩能力障碍和CD之间的联系的见解.
已识别的代谢途径可以作为新型心脏保护疗法的目标,以减少创伤死亡率.

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