Critical care : the official journal of the Critical Care Forum
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Biguanide poisoning is associated with lactic acidosis. The exact mechanism of biguanide-induced lactic acidosis is not well understood. In the previous issue of Critical Care, Protti and colleagues demonstrated that biguanide-induced lactic acidosis may be due in part to a reversible inhibition of mitochondrial respiration. Thus, in the absence of an antidote, increased drug elimination through dialysis is logical.
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Studies have demonstrated that optimising the circulating volume reduces morbidity after major surgery. This optimisation is usually achieved through maximisation of the stroke volume guided by oesophageal Doppler. New monitoring parameters of preload responsiveness using information from the arterial trace are now showing some promise in achieving the same goal. The present commentary examines these new parameters with respect to improving outcomes for the high-risk surgical patient.
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Comparative Study
PD-L1 blockade improves survival in experimental sepsis by inhibiting lymphocyte apoptosis and reversing monocyte dysfunction.
Lymphocyte apoptosis and monocyte dysfunction play a pivotal role in sepsis-induced immunosuppression. Programmed death-1 (PD1) and its ligand programmed death ligand-1 (PD-L1) exert inhibitory function by regulating the balance among T cell activation, tolerance, and immunopathology. PD-1 deficiency or blockade has been shown to improve survival in murine sepsis. However, PD-L1 and PD-1 differ in their expression patterns and the role of PD-L1 in sepsis-induced immunosuppression is still unknown. ⋯ PD-L1 blockade exerts a protective effect on sepsis at least partly by inhibiting lymphocyte apoptosis and reversing monocyte dysfunction. Anti-PD-L1 antibody administration may be a promising therapeutic strategy for sepsis-induced immunosuppression.
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During the past decade, there have been an increasing number of studies investigating the precise role of T regulatory cells in human disease. First recognized for their ability to prevent autoimmunity, T regulatory cells control effector CD4+ and CD8+ T lymphocytes and innate immune cells by several different suppressive mechanisms, like cell to cell contact, secretion of inhibitory cytokines and cytolysis. This suppressive function of T regulatory cells could contribute in a similar way to the profound immune dysfunction seen in critical illness whether the latter is due to sepsis or severe injury.
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Comment
Does anesthetic provide similar neuroprotection to therapeutic hypothermia after cardiac arrest?
In the previous issue of Critical Care, Meybohm and colleagues provide evidence to support hypothermia as a kind of therapeutic option for patients suffering cardiac arrest. Although anesthetics had been used to induce hypothermia, sevoflurane post-conditioning fails to confer additional anti-inflammatory effects after cardiac arrest. Further research in this area is warranted.