Critical care : the official journal of the Critical Care Forum
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Acetaminophen (APAP) toxicity is the most common cause of acute liver failure in the US and Europe. Massive hepatocyte necrosis is the predominant feature of APAP-induced acute liver injury (ALI). Liver regeneration is a vital process for survival after a toxic insult, it occurs at a relative late time point after the injurious phase. Currently, N-acetylcysteine (NAC), a glutathione precursor, is the antidote for acetaminophen overdose. However, NAC is effective only for patients who present within hours of an acute overdose, and is less effective for late-presenting patients. It is possible that in delayed patients, previously reduced endogenous glutathione (GSH) level has restored and prolonged treatment with NAC might be toxic and impair liver regeneration. Therefore, we hypothesize that prolonged treatment with NAC impairs liver regeneration in ALI induced by APAP. ⋯ Prolonged treatment with NAC impairs liver regeneration in ALI induced by APAP.
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The anaesthetic agent propofol (2,6-diisopropylphenol) has been shown to be an effective neuroprotective agent in different in vitro models of brain injury induced by oxygen and glucose deprivation. We examined its neuroprotective properties in an in vitro model of traumatic brain injury. ⋯ When used in combination, the dose-dependent neuroprotective effect of propofol is additive to the neuroprotective effect of hypothermia in an in vitro model of traumatic brain injury.
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Advanced glycation endproducts (AGEs) are primarily known as a complication in diabetic patients through their mediation of the inflammatory response. However, a variety of studies have demonstrated enhanced formation of AGEs in cardiovascular disorders. Despite the large number of AGEs produced during the Maillard reaction, recent focus is on the major non-crosslinking AGE Nepsilon-carboxymethyllysine. ⋯ Therefore, AGEs may participate in the inflammatory response related to cardiac dysfunction in critically ill patients. Moreover, life-saving ventilation stimulates AGE formation in these patients. This interesting study raises the question of whether AGEs in critically ill patients are a driving force of the disease.