吸烟使创伤后的代谢组学反应致敏。
Smoking primes the metabolomic response in trauma.
机构信息
From the Department of Gastrointestinal, Trauma, and Endocrine Surgery (C.E., A.D., T.S., O.T., W.H., S.M., P.S., C.C.S., M.J.C.), University of Colorado; Ernest E. Moore Shock Trauma Center (E.E.M.), Denver Health; and Division of Pulmonary, Critical Care, Allergy and Sleep Medicine, Departments of Medicine (C.S.C.) and Anesthesia (C.S.C.), University of Colorado, Aurora, Colorado.
出版信息
J Trauma Acute Care Surg. 2024 Jul 1;97(1):48-56. doi: 10.1097/TA.0000000000004318. Epub 2024 Mar 29.
INTRODUCTION
Smoking is a public health threat because of its well-described link to increased oxidative stress-related diseases including peripheral vascular disease and coronary artery disease. Tobacco use has been linked to risk of inpatient trauma morbidity including acute respiratory distress syndrome; however, its mechanistic effect on comprehensive metabolic heterogeneity has yet to be examined.
METHODS
Plasma was obtained on arrival from injured patients at a Level 1 trauma center and analyzed with modern mass spectrometry-based metabolomics. Patients were stratified by nonsmoker, passive smoker, and active smoker by lower, interquartile, and upper quartile ranges of cotinine intensity peaks. Patients were substratified by high injury/high shock (Injury Severity Score, ≥15; base excess, <-6) and compared with healthy controls. p Value of <0.05 following false discovery rate correction of t test was considered significant.
RESULTS
Forty-eight patients with high injury/high shock (7 nonsmokers [15%], 25 passive smokers [52%], and 16 active smokers [33%]) and 95 healthy patients who served as controls (30 nonsmokers [32%], 43 passive smokers [45%], and 22 active smokers [23%]) were included. Elevated metabolites in our controls who were active smokers include enrichment in chronic inflammatory and oxidative processes. Elevated metabolites in active smokers in high injury/high shock include enrichment in the malate-aspartate shuttle, tyrosine metabolism, carnitine synthesis, and oxidation of very long-chain fatty acids.
CONCLUSION
Smoking promotes a state of oxidative stress leading to mitochondrial dysfunction, which is additive to the inflammatory milieu of trauma. Smoking is associated with impaired mitochondrial substrate utilization of long-chain fatty acids, aspartate, and tyrosine, all of which accentuate oxidative stress following injury. This altered expression represents an ideal target for therapies to reduce oxidative damage toward the goal of personalized treatment of trauma patients.
LEVEL OF EVIDENCE
Prognostic and Epidemiological; Level IV.
简介
吸烟是一种公共健康威胁，因为它与增加的氧化应激相关疾病有明确的联系，包括外周血管疾病和冠状动脉疾病。烟草使用与住院创伤发病率的风险相关，包括急性呼吸窘迫综合征;然而，其对全面代谢异质性的机制影响尚未被研究。
方法
在一级创伤中心，从受伤患者到达时获得血浆，并使用现代基于质谱的代谢组学进行分析。患者根据可替宁强度峰值的下四分位数、四分位数和上四分位数范围分为非吸烟者、被动吸烟者和主动吸烟者。患者按高损伤/高休克（损伤严重程度评分，≥15；基础不足，<-6）分层，并与健康对照进行比较。t 检验经假发现率校正后 p 值<0.05 被认为具有统计学意义。
结果
共纳入 48 例高损伤/高休克患者（7 例非吸烟者[15%]、25 例被动吸烟者[52%]和 16 例主动吸烟者[33%]）和 95 例健康对照者（30 例非吸烟者[32%]、43 例被动吸烟者[45%]和 22 例主动吸烟者[23%]）。我们的对照组中主动吸烟者的代谢物升高包括慢性炎症和氧化过程的富集。高损伤/高休克的主动吸烟者中升高的代谢物包括苹果酸-天冬氨酸穿梭、酪氨酸代谢、肉碱合成和极长链脂肪酸氧化的富集。
结论
吸烟会导致氧化应激状态，导致线粒体功能障碍，这会加重创伤的炎症环境。吸烟与创伤后长链脂肪酸、天冬氨酸和酪氨酸的线粒体底物利用受损有关，所有这些都加剧了氧化应激。这种改变的表达代表了减少氧化损伤的理想治疗靶点，以实现创伤患者的个体化治疗目标。
证据水平
预后和流行病学；IV 级。
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