Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Sepsis-associated acute kidney injury (SA-AKI) is associated with significant morbidity and mortality. Immune dysregulation is a hallmark of sepsis, with important contributions to organ dysfunction including injury and repair mechanisms in AKI. Macrolide antibiotics, such as azithromycin, have previously demonstrated in preclinical models a myriad of immunomodulatory effects that may benefit critically ill patients with SA-AKI. The aim of this study was to determine if early receipt of azithromycin in SA-AKI is associated with a reduction in major adverse kidney events (MAKE) at hospital discharge. ⋯ Early exposure to azithromycin in SA-AKI is independently associated with lower odds of MAKE at hospital discharge.
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Sepsis-induced cardiomyopathy (SIC) is a major contributing factor for morbidity and mortality in sepsis. Accumulative evidence has suggested that cardiac mitochondrial oxidative phosphorylation is attenuated in sepsis, but the underlying molecular mechanisms remain incompletely understood. ⋯ These data demonstrate a broad mitochondrial protein remodeling, PDH inactivation and impaired pyruvate-fueled oxidative phosphorylation during SIC, and provide a molecular framework for further exploration.
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Hemorrhagic shock is the important factor for causing death of trauma and war injuries. However, pathophysiological characteristics and underlying mechanism in hemorrhagic shock with hot environment remain unclear. ⋯ Hot environment accelerated the death of hemorrhagic shock rats, which was related to the disorder of internal environment, the increase of inflammatory and stress factors. Furthermore, moderate hypothermic (10°C) fluid resuscitation was suitable for the treatment of hemorrhagic shock in hot environment.
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To investigate the activity of key rate-limiting enzymes of glucose metabolism after restoration of spontaneous circulation (ROSC), to explore the potential pathophysiological mechanism of impaired myocardial energy metabolism after cardiopulmonary resuscitation (CPR). ⋯ Lowered key rate-limiting enzymes activity in glucose metabolism resulted in impairment of energy production in the early stage of ROSC, but partially recovered in 24 h. This process has a role in the mechanism of impaired myocardial energy metabolism after CPR. This investigation might shed light on new strategies to treat post resuscitation myocardial dysfunction.
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Acute respiratory distress syndrome (ARDS) is a life-threatening condition characterized by increased permeability of the alveolar-capillary barrier and impaired alveolar fluid clearance. Resolvin E1 (RvE1) is a specialized pro-resolving mediator derived endogenously from omega-3-polyunsaturated fatty acids. RvE1 (10 μg/kg i.v.) was injected to rats 6 h post-lipopolysaccharide (LPS) (14 mg/kg) induction. ⋯ In addition, RvE1 significantly increased the expression of phosphorylated AKT, SGK1, and phosphorylated Nedd4-2 in LPS-stimulated primary alveolar type II cells. The effects of RvE1 were abrogated by blocking phosphatidylinositide3'-kinase (PI3K) and SGK1 with LY294002 and GSK650394, respectively. In summary, RvE1 upregulated ENaC and NKA expression by activating PI3K/AKT/SGK1 pathway to promote alveolar fluid clearance, suggesting that RvE1 may be a potentially effective drug for ARDS treatment.