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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Perftoran, which has been rebranded as Vidaphor for marketing in North America, is an emulsion of perfluorocarbons in a surfactant and electrolyte mixture. It was developed in Russia as an oxygen-carrying intravenous plasma additive for hemorrhagic anemia and ischemic conditions from various etiologies. It was approved for clinical use in Russia in 1996 and used by the Russian Armed Forces and in civilian medical care. ⋯ It has been safely administered to more patients than any oxygen carrier currently under development. A newly formed United States Corporation (FluorO2 Therapeutics, Inc.) intends to manufacture the product in the United States under GMP standards and make it available for clinical use in Mexico and Latin America and pursue research to support eventual approval in the United States for human and veterinary use. This article will briefly review key information about this product and provide references for the interested reader.
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Excessive microvascular permeability is a serious complication following hemorrhagic shock and resuscitation (HSR). S1P has been shown to ameliorate microvascular leakage in a model of combined alcohol intoxication and HSR. In the current study, we tested the hypothesis that S1P reduces HSR-induced microvascular leakage by preserving endothelial cell junctional structure and the endothelial glycocalyx through the protection of mitochondrial function. ⋯ S1P treatment during HSR also protects against mitochondrial membrane depolarization. S1P also protects against mitochondrial dysfunction-induced endothelial barrier dysfunction and glycocalyx degradation by acting through mitochondrial complex III. Taken together, our data indicate that S1P protects against HSR-induced mitochondrial dysfunction in endothelial cells, which in turn improves the structure of the endothelial glycocalyx after HSR and allows for better junctional integrity to the prevention of excess microvascular permeability.
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Mechanical ventilation is known to activate oxidative stress and proteolytic pathways in the diaphragm. Trauma by inducing inflammation and activating proteolytic pathways may potentiate the effects of mechanical ventilation on the diaphragm. In a blunt chest trauma with concomitant injuries we tested the hypothesis that trauma via inflammation further activates the proteolytic pathways and worsens atrophy in the diaphragm. ⋯ Trauma and mechanical ventilation induced proteolysis and atrophy in the diaphragm, but only polytrauma induced an inflammatory response in the diaphragm. The additional traumatic inflammatory stimulus did not increase the levels of the prementioned variables. These data underline that inflammation is not a major contributor to ventilator-induced diaphragmatic dysfunction.
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Clinical Trial Observational Study
The Effect of Nutrition on Early Stress-Induced Hyperglycemia, Serum Insulin Levels, and Exogenous Insulin Administration in Critically Ill Patients with Septic Shock: A Prospective Observational Study.
Stress-induced hyperglycemia is common among septic shock patients. Nutritional support influences glucose homeostasis but this effect has never been studied in septic shock. We aimed to determine the course of hyperglycemia and serum insulin levels in critically ill septic shock patients and to address the effects of caloric intake on glycemia, insulin levels, and exogenous insulin requirements. ⋯ In patients with septic shock marked reduced serum insulin levels can be observed during the first 36 h after intensive care unit (ICU) admission that have to be compensated by exogenous insulin administration, a phenomenon gradually improving after 36 h. Feeding is positively associated with exogenous insulin requirements. These results suggest that strategies to manage stress-induced hyperglycemia in patients with septic shock should consider frequent glycemic monitoring, conservative insulin dosing to prevent hypoglycemia when insulin resistance disappears, and slow progressive nutrition support during the early ICU phase as caloric loading may worsen hyperglycemia. This approach may attenuate the risk of glucose variability, hypo- and hyperglycemia and associated poor outcomes.
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Antithrombin (AT) III physiological levels are decreased during septic shock and supplementation therapy could therefore be beneficial. ⋯ In our model of endotoxic shock, a single low dose of recombinant human AT did not prevent DIC occurrence, severity, inflammatory profile, or hemodynamic alterations.