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中华危重症医学杂志(电子版) ›› 2018, Vol. 11 ›› Issue (02) : 133 -138. doi: 10.3877/cma.j.issn.1674-6880.2018.02.014

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综述

ICU获得性肌无力病理生理机制的研究进展
刘蕾1, 李景辉1,(), 刘芙蓉1, 曹玉芳1   
  1. 1. 570208 海口,中南大学湘雅医学院附属海口医院重症医学科
  • 收稿日期:2017-10-13 出版日期:2018-04-01
  • 通信作者: 李景辉
  • 基金资助:
    海口市重点科技计划项目(2012-068)
  • Received:2017-10-13 Published:2018-04-01
引用本文:

刘蕾, 李景辉, 刘芙蓉, 曹玉芳. ICU获得性肌无力病理生理机制的研究进展[J]. 中华危重症医学杂志(电子版), 2018, 11(02): 133-138.

[1]
杨娜,李维勤. 慢重症新诊断标准及治疗进展[J/CD]. 中华危重症医学杂志(电子版),2016,9(3):197-200.
[2]
Kramer CL. Intensive care unit-acquired weakness[J]. Neurol Clin, 2017, 35 (4): 723.
[3]
Bierbrauer J, Koch S, Olbricht C, et al. Early type Ⅱ fiber atrophy in intensive care unit patients with nonexcitable muscle membrane[J]. Crit Care Med, 2012, 40 (2): 647-650.
[4]
Kraner SD, Novak KR, Wang Q, et al. Altered sodium channel-protein associations in critical illness myopathy[J]. Skelet Muscle, 2012, 2 (1): 17.
[5]
Koesters A, Engisch KL, Rich MM. Decreased cardiac excitability secondary to reduction of sodium current may be a significant contributor to reduced contractility in a rat model of sepsis[J]. Crit Care, 2014, 18 (2): R54.
[6]
Nardelli P, Vincent JA, Powers R, et al. Reduced motor neuron excitability is an important contributor to weakness in a rat model of sepsis[J]. Exp Neurol, 2016 (282): 1-8.
[7]
Friedrich O, Reid MB, van den Berghe G, et al. The sick and the weak: neuropathies/myopathies in the critically ill[J]. Physiol Rev, 2015, 95 (3): 1025-1109.
[8]
Guillouet M, Gueret G, Rannou F, et al. Tumor nec-rosis factor-alpha downregulates sodium current in skeletal muscle by protein kinase C activation: involvement in critical illness polyneuromyopathy[J]. Am J Physiol Cell Physiol, 2011, 301 (5): C1057-C1063.
[9]
Llano-Diez M, Cheng A J, Jonsson W, et al. Impaired Ca2+ release contributes to muscle weakness in a rat model of critical illness myopathy[J]. Crit Care, 2016, 20 (1): 254.
[10]
Kraner SD, Wang Q, Novak KR, et al. Upregulation of the CaV 1.1-ryanodine receptor complex in a rat model of critical illness myopathy[J]. Am J Physiol Reg I, 2011, 300 (6): R1384-R1391.
[11]
Zink W, Kaess M, Hofer S, et al. Alterations in in-tracellular Ca2+-homeostasis of skeletal muscle fibers during sepsis[J]. Crit Care Med, 2008, 36 (5): 1559-1563.
[12]
Friedrich O, Yi B, Edwards JN, et al. IL-1α reversi-bly inhibits skeletal muscle ryanodine receptor. A novel mechanism for critical illness myopathy?[J]. Am J Resp Cell Mol, 2014, 50 (6): 1096-1106.
[13]
刘雪云,李高权,徐守宇. 废用性肌萎缩的蛋白质合成和降解途径[J]. 中国运动医学杂志,2013,32(7):654-657.
[14]
Sacheck JM, Hyatt JK, Raffaello A, et al. Rapid dis-use and denervation atrophy involve transcriptional changes similar to those of muscle wasting during systemic diseases[J]. Faseb J, 2007, 21 (1): 140-155.
[15]
Dupont-Versteegden EE, Strotman BA, Gurley CM, et al. Nuclear translocation of EndoG at the initiation of disuse muscle atrophy and apoptosis is specific to myonuclei[J]. Am J Physiol Regul Integr Comp Physiol, 2006, 291 (6): R1730-R1740.
[16]
Hu NF, Chang H, Du B, et al. Tetramethylpyrazine ameliorated disuse-induced gastrocnemius muscle atrophy in hindlimb unloading rats through suppression of Ca2+/ROS-mediated apoptosis[J]. Appl Physiol Nutr Metab, 2017, 42 (2): 117-127.
[17]
Wan J, Chen D, Yu B, et al. Leucine protects against skeletal muscle atrophy in lipopolysaccharide-challenged rats[J]. J Med Food, 2017, 20 (1): 93-101.
[18]
Belova SP, Shenkman BS, Kostrominova TY, et al. Paradoxical effect of IKK inhibition on the expression of E3 ubiquitin ligases and unloading-induced skeletal muscle atrophy[J]. Physiol Rep, 2017, 5 (16): e13291.
[19]
屈惠莹,包翠芬,于迪,等. 地塞米松诱导的危重病性肌病大鼠骨骼肌Beclin1、LC3的表达[J]. 中国临床解剖学杂志,2017(3):276-281.
[20]
Banduseela VC, Chen YW, Kultima HG, et al. Impa-ired autophagy, chaperone expression, and protein synthesis in response to critical illness interventions in porcine skeletal muscle[J]. Physiol Genomics, 2013, 45 (12): 477-486.
[21]
Kang C, Yeo D, Ji LL. Muscle immobilization activates mitophagy and disrupts mitochondrial dynamics in mice[J]. Acta Physiol (Oxf), 2016, 218 (3): 188-197.
[22]
Han B, Tong J, Zhu MJ, et al. Insulin-like growth factor-1 (IGF-1) and leucine activate pig myogenic satellite cells through mammalian target of rapamycin (mTOR) pathway[J]. Mol Reprod Dev, 2008, 75 (5): 810-817.
[23]
Bloch SA, Lee JY, Wort SJ, et al. Sustained elevation of circulating growth and differentiation factor-15 and a dynamic imbalance in mediators of muscle homeostasis are associated with the development of acute muscle wasting following cardiac surgery[J]. Crit Care Med, 2013, 41 (4): 982-989.
[24]
Bloch SA, Lee JY, Syburra T, et al. Increased expression of GDF-15 may mediate ICU-acquired weakness by down-regulating muscle microRNAs[J]. Thorax, 2015, 70 (3): 219-228.
[25]
孙文武,毛恩强. 微循环变化对于脓毒症患者液体复苏治疗的意义[J/CD]. 中华危重症医学杂志(电子版),2016,9(3):201-204.
[26]
Pollock N, Staunton CA, Vasilaki A, et al. Denervated muscle fibers induce mitochondrial peroxide generation in neighboring innervated fibers: role in muscle aging[J]. Free Radica Biol Med, 2017 (112): 84-92.
[27]
Wagatsuma A, Kotake N, Mabuchi K, et al. Express-ion of nuclear-encoded genes involved in mitochondrial biogenesis and dynamics in experimentally denervated muscle[J]. J Physiol Biochem, 2011, 67 (3): 359-370.
[28]
Tavi P, Westerblad H. The role of in vivo Ca2+ signals acting on Ca2+-calmodulin-dependent proteins for skeletal muscle plasticity[J]. J Physiol, 2011, 589 (21): 5021-5031.
[29]
Kalamgi RC, Salah H, Gastaldello S, et al. Mechano-signalling pathways in an experimental intensive critical illness myopathy model[J]. J Physiol, 2016, 594 (15): 4371-4388.
[30]
Rocheteau P, Chatre L, Briand D, et al. Sepsis indu-ces long-term metabolic and mitochondrial muscle stem cell dysfunction amenable by mesenchymal stem cell therapy[J]. Nat Commun, 2015, 6 (24): 10145.
[31]
Derde S, Vanhorebeek I, Ververs E, et al. Increasing intravenous glucose load in the presence of normoglycemia: effect on outcome and metabolism in critically ill rabbits[J]. Crit Care Med, 2010, 38 (2): 602-611.
[32]
Weber-Carstens S, Schneider J, Wollersheim T, et al. Critical illness myopathy and GLUT4[J]. Am J Resp Crit Care, 2013, 187 (4): 387-396.
[33]
Ono Y, Sakamoto K. Lipopolysaccharide inhibits myo-genic differentiation of C2C12 myoblasts through the Toll-like receptor 4-nuclear factor-kappaB signaling pathway and myoblast-derived tumor necrosis factor-alpha[J]. PLoS One, 2017, 12 (7): e182040.
[34]
Munoz-Canoves P, Scheele C, Pedersen BK, et al. Interleukin-6 myokine signaling in skeletal muscle: a double-edged sword?[J]. Febs J, 2013, 280 (17): 4131-4148.
[35]
Stasko SA, Hardin BJ, Smith JD, et al. TNF signals via neuronal-type nitric oxide synthase and reactive oxygen species to depress specific force of skeletal muscle[J]. J Appl Physiol, 2013, 114 (11): 1629-1636.
[36]
Janssen SP, Gayan-Ramirez G, van den Bergh A, et al. Interleukin-6 causes myocardial failure and skeletal muscle atrophy in rats[J]. Circulation, 2005, 111 (8): 996-1005.
[37]
Wieske L, Witteveen E, Petzold A, et al. Neurofilame-nts as a plasma biomarker for ICU-acquired weakness: an observational pilot study[J]. Crit Care, 2014, 18 (1): R18.
[38]
Price DR, Mikkelsen ME, Umscheid CA, et al. Neuro-muscular blocking agents and neuromuscular dysfunction acquired in critical illness: a systematic review and meta-analysis[J]. Crit Care Med, 2016, 44 (11): 2070-2078.
[39]
Nardelli P, Vincent JA, Powers R, et al. Reduced motor neuron excitability is an important contributor to weakness in a rat model of sepsis[J]. Exp Neurol, 2016 (282): 1-8.
[40]
Miura A, Hino H, Uchida K, et al. Peripheral nerve conduction abnormalities precede morphological alterations in an experimental rat model of sepsis[J]. J Anesth, 2016, 30 (6): 961-969.
[41]
Aare S, Radell P, Eriksson LI, et al. Role of sepsis i-n the development of limb muscle weakness in a porcine intensive care unit model[J]. Physiol Genomics, 2012, 44 (18): 865-877.
[42]
Feng L, Liu X, Cao F, et al. Anti-stress effects of ginseng total saponins on hindlimb-unloaded rats assessed by a metabolomics study[J]. J Ethnopharmacol, 2016 (188): 39-47.
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