Wu Jin, Li Shi-Tong
Department of Anesthesiology, First People's Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200080, China.
Chin Med J (Engl). 2015 May 20;128(10):1407-11. doi: 10.4103/0366-6999.156808.
The objective was to evaluate the protective effects of dexmedetomidine (DEX), a selective agonist of α2-adrenergic receptor, on sepsis-induced diaphragm injury and the underlying molecular mechanisms.
The data used in this review were mainly from PubMed articles published in English from 1990 to 2015.
Clinical or basic research articles were selected mainly according to their level of relevance to this topic.
Sepsis could induce severe diaphragm dysfunction and exacerbate respiratory weakness. The mechanism of sepsis-induced diaphragm injury includes the increased inflammatory cytokines and excessive oxidative stress and superfluous production of nitric oxide (NO). DEX can reduce inflammatory cytokines, inhibit nuclear factor-kappaB signaling pathways, suppress the activation of caspase-3, furthermore decrease oxidative stress and inhibit NO synthase. On the basis of these mechanisms, DEX may result in a shorter period of mechanical ventilation in septic patients in clinical practice.
Based on this current available evidence, DEX may produce extra protective effects on sepsis-induced diaphragm injury. Further direct evidence and more specific studies are still required to confirm these beneficial effects.
本研究旨在评估α2肾上腺素能受体选择性激动剂右美托咪定（DEX）对脓毒症诱导的膈肌损伤的保护作用及其潜在分子机制。
本综述所使用的数据主要来自1990年至2015年以英文发表在PubMed上的文章。
主要根据与本主题的相关程度来选择临床或基础研究文章。
脓毒症可导致严重的膈肌功能障碍并加重呼吸肌无力。脓毒症诱导膈肌损伤的机制包括炎性细胞因子增加、过度氧化应激以及一氧化氮（NO）生成过多。DEX可减少炎性细胞因子、抑制核因子-κB信号通路、抑制半胱天冬酶-3的激活，此外还可减轻氧化应激并抑制NO合酶。基于这些机制，在临床实践中DEX可能会使脓毒症患者的机械通气时间缩短。
基于目前可得的证据，DEX可能对脓毒症诱导的膈肌损伤产生额外的保护作用。仍需要进一步的直接证据和更具体的研究来证实这些有益作用。
