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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Clinical evidence supports the existence of a trauma-induced secondary cardiac injury. Experimental research suggests inflammation as a possible mechanism. The study aimed to determine if there was an early association between inflammation and secondary cardiac injury in trauma patients. ⋯ There is an association between hyperacute elevations in inflammatory cytokines with cardiac injury and ACEs in critically injured patients. Biomarker evidence of cardiac injury and inflammation on admission is associated with a higher risk of in-hospital death.
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Inappropriate use of antimicrobial drugs is responsible for therapeutic failures, increased mortality rates, and the emergence of resistance. Antimicrobial activity is determined by intrinsic pharmacokinetics/pharmacodynamics concepts. In critically ill patients, an inappropriate dosing regimen can be caused by the inability of an antimicrobial drug to reach adequate concentrations at the infection site owing to alterations in the drug's pharmacokinetics caused by pathophysiological changes. Understanding these concepts and changes in PK-PD parameters that occur in intensive care unit patients is crucial for the optimization of antimicrobial therapy in these patients.
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Remote ischemic perconditioning (RIPer) and local ischemic postconditioning (IPost) are promising methods to decrease ischemia-reperfusion injury. We tested whether these two methods were effective in reducing infarct size through activation of endoplasmic reticulum (ER) stress response, a potential survival pathway. Rats exposed to myocardial ischemia-reperfusion were allocated to one of six groups: control, no intervention at myocardial reperfusion; IPost, three cycles of 10-s coronary artery occlusion followed by 10-s reperfusion applied at the onset of myocardial reperfusion; RIPer, 10-min limb ischemia followed by 10-min reperfusion initiated during coronary artery occlusion; control + 4-PBA, injection of ER stress inhibitor 4-phenylbutyrate (4-PBA) 1 h before coronary occlusion; IPost + 4-PBA; and RIPer + 4-PBA. ⋯ Furthermore, 4-PBA abolished cardioprotection induced by IPost (infarct size 53.75 ± 3.49 vs. 33.32 ± 3.65%, P < 0.05) but not by RIPer (28.80 ± 10.45% vs. 21.86 ± 3.98%, not statistically significant). GRP78 and cleaved activating transcription factor 6 levels were no longer increased in IPost group after 4-PBA. These findings point to a role for ER stress response in cardioprotection against reperfusion injury in IPost but not RIPer, suggesting differences in cardioprotective mechanisms between local and remote conditioning.
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Sepsis is the main cause of acute kidney injury (AKI) among individuals hospitalized in intensive care units. Acute kidney injury is an independent risk factor for mortality, and its occurrence increases the complexity and cost of treatment. However, the pathophysiological mechanisms of AKI remain unclear. ⋯ Dialysis is the main treatment for AKI. Although there is no clear benefit of any specific dialysis modality, these patients are initially instructed to use continuous dialysis methods, especially for the most severe cases with multiple organ system dysfunctions and for those who display signs of hemodynamic instability. Recent studies demonstrate that patients should receive a dialysis dose of at least 25 mL · kg · h.
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The aim of the study was to evaluate the effects of bolus infusion of hypertonic hydroxyethyl starches (HHESs) and continuous infusion of hypertonic saline (HTS) in the early resuscitation in crush syndrome. ⋯ Bolus infusion of HHES combined with normal saline could be an effective therapy for crush syndrome in the early resuscitation period. However, continuous HTS injection was not seemed to be a suitable choice particularly in the absence of monitoring equipment for serum irons or blood gases (institutional protocol no. ZN5R20110016).