Objective:The objective was to evaluate the protective effects ofdexmedetomidine (DEX),a selective agonist of α2-adrenergic receptor,on sepsis-induced diaphragm injury and the underlying molecular mechanisms.Data Sources:The data used in this review were mainly from PubMed articles published in English from 1990 to 2015.Study Selection:Clinical or basic research articles were selected mainly according to their level of relevance to this topic.Results: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.Conclusions: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.
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