Báo cáo y học: " Bench-to-bedside review: Cytopathic hypoxia"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về y học đề tài: Bench-to-bedside review: Cytopathic hypoxia. | Available online http content 6 6 491 Review Bench-to-bedside review Cytopathic hypoxia Mitchell P Fink Professor and Chairman Department of Critical Care Medicine Watson Chair in Surgery University of Pittsburgh Medical School Pittsburgh Pennsylvania USA Correspondence Mitchell P Fink finkmp@ Published online 12 September 2002 Critical Care 2002 6 491-499 DOI cc1824 This article is online at http content 6 6 491 2002 BioMed Central Ltd Print ISSN 1364-8535 Online ISSN 1466-609X Abstract The rate of oxygen consumption by certain tissues is impaired when mice or rats are injected with lipopolysaccharide. A similar change in the rate of oxygen consumption is observed when Caco-2 human enterocyte-like cells are incubated in vitro with cytomix a cocktail of cytokines containing tumor necrosis factor IL-1P and IFN-y. The decrease in the rate of oxygen consumption is not due to a change in oxygen delivery . on the basis of diminished microvascular perfusion but rather to an acquired intrinsic defect in cellular respiration a phenomenon that we have termed cytopathic hypoxia . A number of different biochemical mechanisms have been postulated to account for cytopathic hypoxia in sepsis including reversible inhibition of cytochrome a a3 by nitric oxide and irreversible inhibition of one or more mitochondrial respiratory complexes by peroxynitrite. Recently however our laboratory has obtained data to suggest that the most important mechanism underlying the development of cytopathic hypoxia is depletion of cellular stores of nicotinamide adenine dinucleotide NAD NADH as a result of activation of the enzyme poly ADP-ribose polymerase-1. If cytopathic hypoxia is important in the pathophysiology of established sepsis and multiorgan dysfunction syndrome then efforts in the future will need to focus on pharmacological interventions designed to preserve normal mitochondrial function and energy production in sepsis. Keywords ATP LPS .

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