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Cardiac dysfunction in sepsis: new theories and clinical implications.

作者信息

Grocott-Mason R M, Shah A M

机构信息

Department of Cardiology, University of Wales College of Medicine, Cardiff, UK.

出版信息

Intensive Care Med. 1998 Apr;24(4):286-95. doi: 10.1007/s001340050570.

DOI:10.1007/s001340050570
PMID:9609405
Abstract
摘要

相似文献

1
Cardiac dysfunction in sepsis: new theories and clinical implications.脓毒症中的心脏功能障碍：新理论与临床意义
Intensive Care Med. 1998 Apr;24(4):286-95. doi: 10.1007/s001340050570.
2
Cardiac dysfunction in septic shock and multiple organ dysfunction syndrome.脓毒性休克和多器官功能障碍综合征中的心脏功能障碍
Crit Care Nurs Q. 1994 Feb;16(4):39-48. doi: 10.1097/00002727-199402000-00006.
3
Cardiac dysfunction in severe sepsis and septic shock.严重脓毒症和脓毒性休克中的心脏功能障碍。
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4
Myocardial dysfunction in sepsis. Recent insights.脓毒症中的心肌功能障碍。最新见解。
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5
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Chest. 2012 Mar;141(3):835. doi: 10.1378/chest.11-2717.
6
[Acute septic cardiomyopathy].[急性脓毒症性心肌病]
Internist (Berl). 1998 May;39(5):467-78. doi: 10.1007/s001080050198.
7
[Diastolic malfunction in sepsis and septic shock].
Anesteziol Reanimatol. 2004 Jul-Aug(4):47-9.
8
Is cell death a prerequisite for cardiac dysfunction during sepsis?细胞死亡是脓毒症期间心脏功能障碍的先决条件吗？
Crit Care Med. 2005 May;33(5):1160-2. doi: 10.1097/01.ccm.0000159727.27059.d2.
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Critical illness polyneuropathy in patients with systemic inflammatory response syndrome or septic shock.全身炎症反应综合征或脓毒性休克患者的重症疾病多发性神经病
Intensive Care Med. 2001 Mar;27(3):613. doi: 10.1007/s001340100850.
10
Cardiovascular dysfunction in sepsis and critical illness.脓毒症和危重症中的心血管功能障碍。
Vet Clin North Am Small Anim Pract. 2011 Jul;41(4):717-26, v. doi: 10.1016/j.cvsm.2011.04.003. Epub 2011 Jun 16.

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Stress cardiomyopathy of the critically ill: Spectrum of secondary, global, probable and subclinical forms.

本文引用的文献

1
Basal release of nitric oxide augments the Frank-Starling response in the isolated heart.一氧化氮的基础释放增强离体心脏的Frank-Starling反应。
Circulation. 1997 Aug 19;96(4):1320-9. doi: 10.1161/01.cir.96.4.1320.
2
Nitric oxide synthase inhibition by L-NAME in leukocytopenic patients with severe septic shock.L-NAME对严重脓毒性休克白细胞减少患者一氧化氮合酶的抑制作用。
Intensive Care Med. 1997 May;23(5):561-6. doi: 10.1007/s001340050373.
3
Left ventricular systolic and diastolic function in septic shock.感染性休克患者的左心室收缩和舒张功能
危重症患者的应激性心肌病：继发性、全身性、可能型和亚临床型的谱系
Indian Heart J. 2018 Jan-Feb;70(1):177-184. doi: 10.1016/j.ihj.2017.04.005. Epub 2017 Apr 19.
4
Role of TFEB Mediated Autophagy, Oxidative Stress, Inflammation, and Cell Death in Endotoxin Induced Myocardial Toxicity of Young and Aged Mice.TFEB介导的自噬、氧化应激、炎症和细胞死亡在脂多糖诱导的年轻和老年小鼠心肌毒性中的作用
Oxid Med Cell Longev. 2016;2016:5380319. doi: 10.1155/2016/5380319. Epub 2016 Apr 21.
5
Hyperdynamic left ventricular ejection fraction in the intensive care unit.重症监护病房中的高动力性左心室射血分数
Crit Care. 2015 Aug 7;19(1):288. doi: 10.1186/s13054-015-1012-8.
6
Propofol infusion syndrome.
Forensic Sci Med Pathol. 2006 Dec;2(4):277-81. doi: 10.1385/FSMP:2:4:277.
7
Prognostic value of troponins in sepsis: a meta-analysis.脓毒症中肌钙蛋白的预后价值：一项荟萃分析。
Intensive Care Med. 2013 Jul;39(7):1181-9. doi: 10.1007/s00134-013-2902-3. Epub 2013 Apr 18.
8
Phospholemman: a novel cardiac stress protein.磷酸烯醇式丙酮酸载体蛋白：一种新型的心脏应激蛋白。
Clin Transl Sci. 2010 Aug;3(4):189-96. doi: 10.1111/j.1752-8062.2010.00213.x.
9
Sepsis-induced cardiomyopathy: a review of pathophysiologic mechanisms.脓毒症性心肌病：病理生理机制的综述。
Heart Fail Rev. 2010 Nov;15(6):605-11. doi: 10.1007/s10741-010-9176-4.
10
Protein phosphatase 2A contributes to the cardiac dysfunction induced by endotoxemia.蛋白磷酸酶2A促成内毒素血症诱导的心脏功能障碍。
Cardiovasc Res. 2009 Apr 1;82(1):67-76. doi: 10.1093/cvr/cvp037. Epub 2009 Feb 6.
Intensive Care Med. 1997 May;23(5):553-60. doi: 10.1007/s001340050372.
4
Nitric oxide can increase heart rate by stimulating the hyperpolarization-activated inward current, I(f).一氧化氮可通过刺激超极化激活内向电流I(f)来提高心率。
Circ Res. 1997 Jul;81(1):60-8. doi: 10.1161/01.res.81.1.60.
5
Leukocytes and decreased left-ventricular contractility during endotoxemia in rabbits.兔内毒素血症期间的白细胞与左心室收缩力降低
Am J Respir Crit Care Med. 1997 Jun;155(6):1977-83. doi: 10.1164/ajrccm.155.6.9196105.
6
Cytokines, nitrite/nitrate, soluble tumor necrosis factor receptors, and procalcitonin concentrations: comparisons in patients with septic shock, cardiogenic shock, and bacterial pneumonia.细胞因子、亚硝酸盐/硝酸盐、可溶性肿瘤坏死因子受体及降钙素原浓度：脓毒性休克、心源性休克及细菌性肺炎患者的比较
Crit Care Med. 1997 Apr;25(4):607-13. doi: 10.1097/00003246-199704000-00009.
7
Partial inhibition of protein synthesis by Pseudomonas exotoxin A deranges catecholamine sensitivity of cultured rat heart myocytes.铜绿假单胞菌外毒素A对蛋白质合成的部分抑制作用扰乱了培养的大鼠心脏心肌细胞的儿茶酚胺敏感性。
J Mol Cell Cardiol. 1997 Feb;29(2):799-811. doi: 10.1006/jmcc.1996.0324.
8
Inhibition of myocardial crossbridge cycling by hypoxic endothelial cells: a potential mechanism for matching oxygen supply and demand?缺氧内皮细胞对心肌横桥循环的抑制作用：一种氧供需匹配的潜在机制？
Circ Res. 1997 May;80(5):688-98. doi: 10.1161/01.res.80.5.688.
9
L-canavanine, an inhibitor of inducible nitric oxide synthase, improves venous return in endotoxemic rats.L-刀豆氨酸是一种诱导型一氧化氮合酶抑制剂，可改善内毒素血症大鼠的静脉回流。
Crit Care Med. 1997 Mar;25(3):469-75. doi: 10.1097/00003246-199703000-00016.
10
Inducible nitric oxide synthase and tumor necrosis factor-alpha in myocardium in human dilated cardiomyopathy.人类扩张型心肌病心肌中诱导型一氧化氮合酶与肿瘤坏死因子-α
J Am Coll Cardiol. 1997 Mar 15;29(4):716-24. doi: 10.1016/s0735-1097(96)00567-0.