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1
Mediators of multiple organ failure.多器官功能衰竭的介质
Intensive Care Med. 1990;16 Suppl 3(Suppl 3):S192-6. doi: 10.1007/BF01709699.
2
Immunologic assessment of host defense impairment in patients with septic multiple organ failure: relationship between complement activation and changes in neutrophil function.脓毒症多器官功能衰竭患者宿主防御功能受损的免疫学评估:补体激活与中性粒细胞功能变化之间的关系
Surgery. 1994 Feb;115(2):145-55.
3
[Immunological assessment of the pathogenesis of septic-MOF: relationship between complement activation and changes in neutrophil functions].[脓毒症多器官功能障碍综合征发病机制的免疫学评估:补体激活与中性粒细胞功能变化之间的关系]
Nihon Geka Gakkai Zasshi. 1991 Sep;92(9):1304-6.
4
Host responses in mediating sepsis and adult respiratory distress syndrome.宿主反应在介导脓毒症和成人呼吸窘迫综合征中的作用。
Semin Respir Infect. 1990 Sep;5(3):233-47.
5
Current theories on the pathophysiology of multiple organ failure after trauma.创伤后多器官衰竭的病理生理学的当前理论。
Injury. 2010 Jan;41(1):21-6. doi: 10.1016/j.injury.2009.07.010.
6
Role of complement in multiorgan failure.补体在多器官功能衰竭中的作用。
Clin Dev Immunol. 2012;2012:962927. doi: 10.1155/2012/962927. Epub 2012 Dec 20.
7
Multiple organ failure: whole body inflammation?多器官功能衰竭:全身炎症反应?
Schweiz Med Wochenschr. 1989 Mar 18;119(11):347-53.
8
The inflammatory basis of trauma/shock-associated multiple organ failure.创伤/休克相关多器官功能衰竭的炎症基础
Inflamm Res. 1998 May;47(5):201-10. doi: 10.1007/s000110050318.
9
sFas and sFas ligand and pediatric sepsis-induced multiple organ failure syndrome.可溶性Fas、可溶性Fas配体与小儿脓毒症诱发的多器官功能衰竭综合征
Pediatr Res. 2002 Dec;52(6):922-7. doi: 10.1203/00006450-200212000-00018.
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Janus face of complement-driven neutrophil activation during sepsis.补体驱动的中性粒细胞在脓毒症中的双面性。
Semin Immunol. 2018 Jun;37:12-20. doi: 10.1016/j.smim.2018.02.004. Epub 2018 Feb 14.

引用本文的文献

1
Plasma cytokines IL-6, IL-8, and IL-10 are associated with the development of acute respiratory distress syndrome in patients with severe traumatic brain injury.血浆细胞因子白细胞介素-6、白细胞介素-8和白细胞介素-10与重度创伤性脑损伤患者急性呼吸窘迫综合征的发生有关。
Crit Care. 2016 Sep 15;20:288. doi: 10.1186/s13054-016-1470-7.
2
Role of lung contusions on posttraumatic inflammatory response and organ dysfunction in traumatized patients.肺挫伤在创伤患者创伤后炎症反应及器官功能障碍中的作用。
Eur J Trauma Emerg Surg. 2009 Oct;35(5):463-9. doi: 10.1007/s00068-009-9123-z. Epub 2009 Sep 17.
3
Towards a unifying, systems biology understanding of large-scale cellular death and destruction caused by poorly liganded iron: Parkinson's, Huntington's, Alzheimer's, prions, bactericides, chemical toxicology and others as examples.从系统生物学角度理解配体结合不良的铁导致的大规模细胞死亡和破坏:以帕金森病、亨廷顿病、阿尔茨海默病、朊病毒、杀菌剂、化学毒理学等为例。
Arch Toxicol. 2010 Nov;84(11):825-89. doi: 10.1007/s00204-010-0577-x. Epub 2010 Aug 17.
4
Cerebral autoregulation is influenced by carbon dioxide levels in patients with septic shock.脑自动调节受感染性休克患者二氧化碳水平的影响。
Neurocrit Care. 2010 Feb;12(1):35-42. doi: 10.1007/s12028-009-9289-6.
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Oxidative mechanisms of brain dysfunction during sepsis.脓毒症时脑功能障碍的氧化机制。
Neurochem Res. 2010 Jan;35(1):1-12. doi: 10.1007/s11064-009-0043-4. Epub 2009 Aug 14.
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Iron behaving badly: inappropriate iron chelation as a major contributor to the aetiology of vascular and other progressive inflammatory and degenerative diseases.铁的不良表现:不适当的铁螯合是血管及其他进行性炎症和退行性疾病病因的主要促成因素。
BMC Med Genomics. 2009 Jan 8;2:2. doi: 10.1186/1755-8794-2-2.
7
Blood-brain barrier breakdown in septic encephalopathy and brain tumours.脓毒症性脑病和脑肿瘤中的血脑屏障破坏
J Anat. 2002 Jun;200(6):639-46. doi: 10.1046/j.1469-7580.2002.00065.x.
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The significance of endotoxin release in experimental and clinical sepsis in surgical patients--evidence for antibiotic-induced endotoxin release?手术患者实验性和临床脓毒症中内毒素释放的意义——抗生素诱导内毒素释放的证据?
Infection. 1998 Mar-Apr;26(2):77-84. doi: 10.1007/BF02767765.
9
Evaluation of definitions and parameters for sepsis assessment in patients after cardiac surgery.心脏手术后患者脓毒症评估的定义和参数评价
Infection. 1994 Jan-Feb;22(1):8-17. doi: 10.1007/BF01780757.
10
Sepsis and septic shock. II. Treatment.脓毒症与脓毒性休克。二、治疗
Support Care Cancer. 1995 Mar;3(2):111-9. doi: 10.1007/BF00365850.

本文引用的文献

1
Control of vascular permeability by polymorphonuclear leukocytes in inflammation.炎症中多形核白细胞对血管通透性的控制
Nature. 1981 Feb 19;289(5799):646-50. doi: 10.1038/289646a0.
2
Leukocytes are required for increased lung microvascular permeability after microembolization in sheep.绵羊微栓塞后肺微血管通透性增加需要白细胞。
Circ Res. 1981 Mar;48(3):344-51. doi: 10.1161/01.res.48.3.344.
3
Effect of nonviable tissue and abscesses on complement depletion and the development of bacteremia.无活力组织和脓肿对补体消耗及菌血症发生的影响。
J Trauma. 1982 Jul;22(7):527-32. doi: 10.1097/00005373-198207000-00001.
4
Increase in microvascular permeability induced by enzymatically generated free radicals. I. In vivo study.酶促产生的自由基诱导的微血管通透性增加。I. 体内研究。
Microvasc Res. 1981 Nov;22(3):239-54. doi: 10.1016/0026-2862(81)90095-9.
5
Complement activation in patients at risk of developing the adult respiratory distress syndrome.有发生成人呼吸窘迫综合征风险的患者体内的补体激活
Am Rev Respir Dis. 1984 Dec;130(6):1058-64. doi: 10.1164/arrd.1984.130.6.1058.
6
Interleukin-1.白细胞介素-1
Rev Infect Dis. 1984 Jan-Feb;6(1):51-95. doi: 10.1093/clinids/6.1.51.
7
Anaphylatoxin generation in multisystem organ failure.多系统器官衰竭中的过敏毒素生成
J Trauma. 1984 Dec;24(12):1038-43. doi: 10.1097/00005373-198412000-00006.
8
Human C5a des Arg increases vascular permeability.人C5a去精氨酸产物可增加血管通透性。
J Immunol. 1981 Dec;127(6):2376-80.
9
Association of complement activation and elevated plasma-C5a with adult respiratory distress syndrome. Pathophysiological relevance and possible prognostic value.补体激活及血浆C5a升高与成人呼吸窘迫综合征的关联。病理生理相关性及可能的预后价值。
Lancet. 1980 May 3;1(8175):947-9. doi: 10.1016/s0140-6736(80)91403-8.
10
Sepsis complicating the acute respiratory distress syndrome.脓毒症并发急性呼吸窘迫综合征。
Surg Gynecol Obstet. 1972 Dec;135(6):865-9.

多器官功能衰竭的介质

Mediators of multiple organ failure.

作者信息

Goris R J

机构信息

Department of General Surgery, University Hospital St. Radboud, Nijmegen, The Netherlands.

出版信息

Intensive Care Med. 1990;16 Suppl 3(Suppl 3):S192-6. doi: 10.1007/BF01709699.

DOI:10.1007/BF01709699
PMID:2289989
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7095330/
Abstract

Multiple Organ Failure (MOF) has largely been attributed to bacterial sepsis, though conclusive evidence of an essential role for bacteria and/or their endotoxins is still lacking. On the other hand, MOF and the clinical syndrome of sepsis may be aseptically induced in germ-free animals. This paper reviews the evidence that excessive activation of endogenous humoral mediators and inflammatory cells may cause this highly lethal syndrome.

摘要

多器官功能衰竭(MOF)在很大程度上被归因于细菌性败血症,尽管仍缺乏关于细菌和/或其内毒素起关键作用的确凿证据。另一方面,MOF和败血症临床综合征可在无菌动物中无菌诱导产生。本文综述了内源性体液介质和炎症细胞过度激活可能导致这种高致死性综合征的证据。