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脓毒症线粒体功能障碍研究进展 被引量：2

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摘要 脓毒症是机体对感染的一种全身性炎症反应，进一步发展可导致感染性休克和多器官功能障碍综合征（multiPleo organ dysfunctionsyndrome，MODS）。线粒体是直接利用氧气制造能量的部位．90％以上的氧气被线粒体消耗掉。线粒体能为细胞的生命活动提供场所．有细胞的“动力工厂”之称。其损伤与脓毒症的发病机制有关。
作者 骆祖骞 钱传云
机构地区 昆明医学院第一附属医院急诊ICU
出处 《实用医学杂志》 CAS 北大核心 2011年第8期1330-1332,共3页 The Journal of Practical Medicine
关键词 线粒体功能障碍 脓毒症 多器官功能障碍综合征 全身性炎症反应 感染性休克 生命活动 发病机制 氧气
分类号 R459.7 [医药卫生—急诊医学]
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参考文献20

  • 1Protti A,Singer M. Bench-to-bedside review:potential strategies to Protect to rerverse mitcohondiral dysfunction in sepsis- induced organ fafiluer [J]. Critical care,2006, 10(5):228.
  • 2Spronk P E, Kanoore-FAlul V S, Lace C. Mierocirculatory and mitochondrial distress Syndrome (MMDS):a new look at sepsis [J]. Intensive Care Emergency Medicine,2004,42(1 ):47-67.
  • 3Victor M, Victor, Juan V. Esplugues, Antonio Hemdndez- Mijaresl, and Milagros Rochal : Oxidative Stress andMitochondrial Dysfunction in Sepsis:A Potential Therapy with Mitochondria-Targeted Antioxidants [ J ]. Infectious Disorders- Drug Targets, 2009,9 : 376-389.
  • 4Boczkowski J, Poderoso J J, Motterlini R. CO-metal interaction : Vital signaling from a lethal gas.Trends in biochemical sciences, 2006 Nov; 31 ( 11 ) : 614-621. Epub 2006, 22.
  • 5Snliman H B, Carraway M S, Ali A S, et al. The CO/HO system reverses inhibition of mitoehondfial biogenesis and prevents routine doxorubicin cardiomyopathy [J]. J Clin Invest, 2007,117 (12) : 3730-3741.
  • 6Lancel S, Hassoun S M, Favory R, et 81. Carbon Monoxide Rescues Mice from Lethal Sepsis by Supporting Mitochondrial Energetic Metabolism and Activating Mitoehondfial Biogenesis [J]. J Pharmacol Exp Ther, 2009,329(2):641-649.
  • 7Zhang W J, Wei H, Hagen T, et al. Alpha-lipoic acid attenuates LPS-induced inflammatory responses by activating the phosphoinositide 3-kinase/AkT signaling pathway [J]. Proc Natl Acad Sci U S A,2007,104(10):4077-4082.
  • 8Virginia Vanasco, Maria Cecilia Cimolai, Pablo Evelson &Silvia Alvarez The oxidative stress and the mitochondrial dysfunction caused by endotoxemia are prevented by a-lipoic acid [J]. Free Radical Research, 2008, 42(9): 815-823.
  • 9Murphy M P, Smith R A J. Targeting antioxidants to mitochondfia by conjugation to lipophilic cations [J]. Annu Rev Pharmacol Toxicol, 2007, 47 : 629-656.
  • 10Ross M F, Prime T A, Abakumova I, et al. Rapid and extensive uptake and activation of hydrophobie triphenylpho- sphonium cations within cells [J]. Biochem J, 2008,411 (3): 633-645.

同被引文献45

  • 1俞国峰,郑霞,方强.辛伐他汀对脓毒症大鼠血清肿瘤坏死因子α及一氧化氮表达的影响[J].中国老年学杂志,2014,34(6):1593-1595. 被引量：1
  • 2骆建军,方强,方雪玲,戚晓平,周博武.脓毒症患者肠道黏膜通透性的临床研究[J].中国急救医学,2007,27(9):789-792. 被引量：13
  • 3Rodriguez-Gonzalez R, Martfn-BarrasaJL, Ramos-Nuez A, et al. Multiple system organ response induced by hyperoxia in a clinically relevant animal model of sepsis[J]. Shock, 2014, 42 (2) : 148 -153.
  • 4Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock, 2012[J]. Intensive Care Med, 2013, 39(2): 165 -228.
  • 5DiGiandooHDco A, Veach RA, ZienkiewiczJ. The "genomic stoon" induced hy bacterial endotoxin is calmed by a nuclear transport modifier that attenuates localized and systemic inflammation[J/OA]. PLoS One, 2014,9(10): el10183.
  • 6Aslami H, Pulskens WP, Kuipers MT, et al. Hydrogen sulfide donor NaHS reduces organ injury in a rat model of pneumococcal pneumosepsis, associated with improved bio-energetic status[J/OA]. PLoS One, 2013, 8(5): e63497.
  • 7Lin X, Lee D, Wu D. Sabiporide improves cardiovascular function and attenuates organ injury from severe sepsis[J].J Surg Res, 2014,188(1): 231-237.
  • 8Gandhimjan RK, Meng S, Chandramoorthy HC, et al. Blockade of NOX2 and STIMI signaling limits lipopolysaccharide-induced vascular inflammation[J] .J Clin Invest, 2013, 123 (2): 887 -902.
  • 9Coletta C, M6dis K, Olah G, et al. Endothelial dysfunction is a potential contributor to multiple organ failure and mortality in aged mice subjected to septic shock: preclinical studies in a murine model of cecal ligation and puncture[J/OL]. Crit Care, 2014,18(5): 511.
  • 10Correa TD,Jeger V, Pereira AI, et al. Angiotensin II in septic shock: effects on tissue perfusion, organ function, and mitochondrial respiration in a porcine model of fecal peritonitis[J/OL]. Crit Care Med, 2014, 42(8): e550 -e559.

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实用医学杂志
2011年 第8期

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