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对损伤的非特异性炎症反应。

The nonspecific inflammatory response to injury.

作者信息

Mayers I, Johnson D

机构信息

Department of Medicine, University of Alberta, Edmonton.

出版信息

Can J Anaesth. 1998 Sep;45(9):871-9. doi: 10.1007/BF03012222.

DOI:10.1007/BF03012222
PMID:9818111
Abstract

PURPOSE

The role of the nonspecific inflammatory response in causing injury related to surgery has become better understood over the last decade. There are complex interactions between neutrophils, cytokines and nitric oxide metabolites that may cause organ injury following surgery. The purpose of this review is to summarize some of the processes causing injury through these nonspecific pathways.

METHODS

A review of the medical and anaesthetic literature related to inflammation, neutrophils and pro-inflammatory cytokines were performed using Medline. Bibliographies of relevant articles were searched and additional articles were then selected and reviewed.

RESULTS

Pro-inflammatory cytokines, such as tumour necrosis factor, are released in response to a variety of noxious stimuli (e.g. burns, sepsis, or CABG surgery). These cytokines cause activation of neutrophils with increased upregulation of adhesion complexes on neutrophils and vascular endothelium. Nitric oxide synthase activity is also increased with a resultant increased production of nitric oxide. The increased nitric oxide concentration in the presence of superoxide free radicals secreted by activated neutrophils forms peroxynitrite, a more reactive and toxic molecule. Once this process is initiated, diffuse organ injury can result. Although some information related to specific anaesthetics is available, firm recommendations related to clinical practice cannot be made.

CONCLUSIONS

There is a complex interplay of inflammatory mediators that can cause injury. Although specific clinical applications for manipulating these pathways are not yet generally available, this area holds promise to develop new techniques to improve outcomes following surgery.

摘要

目的

在过去十年中,非特异性炎症反应在手术相关损伤中所起的作用已得到更好的理解。中性粒细胞、细胞因子和一氧化氮代谢产物之间存在复杂的相互作用,这些相互作用可能导致术后器官损伤。本综述的目的是总结一些通过这些非特异性途径导致损伤的过程。

方法

使用Medline对与炎症、中性粒细胞和促炎细胞因子相关的医学和麻醉学文献进行综述。检索相关文章的参考文献,然后选择并审阅其他文章。

结果

促炎细胞因子,如肿瘤坏死因子,会因各种有害刺激(如烧伤、败血症或冠状动脉旁路移植术)而释放。这些细胞因子会导致中性粒细胞活化,中性粒细胞和血管内皮上的黏附复合物上调增加。一氧化氮合酶活性也会增加,从而导致一氧化氮生成增加。在活化的中性粒细胞分泌的超氧自由基存在的情况下,一氧化氮浓度增加会形成过氧亚硝酸盐,这是一种更具反应性和毒性的分子。一旦这个过程开始,就可能导致弥漫性器官损伤。虽然有一些关于特定麻醉剂的信息,但无法给出与临床实践相关的明确建议。

结论

炎症介质之间存在复杂的相互作用,可导致损伤。虽然目前一般还没有用于操纵这些途径的特定临床应用,但该领域有望开发新技术以改善术后结局。

相似文献

1
The nonspecific inflammatory response to injury.对损伤的非特异性炎症反应。
Can J Anaesth. 1998 Sep;45(9):871-9. doi: 10.1007/BF03012222.
2
Cardiopulmonary bypass-induced inflammation: is it important?体外循环诱导的炎症:它重要吗?
J Cardiothorac Vasc Anesth. 1998 Apr;12(2 Suppl 1):21-5.
3
[Free radicals and antioxidants: physiology, human pathology and therapeutic aspects (part II)].[自由基与抗氧化剂:生理学、人类病理学及治疗学方面(第二部分)]
Therapie. 1998 Jul-Aug;53(4):315-39.
4
Inhibition of nitric oxide synthase attenuates peroxynitrite generation, but augments neutrophil accumulation in hepatic ischemia-reperfusion in rats.一氧化氮合酶的抑制作用可减弱过氧亚硝酸盐的生成,但会增加大鼠肝脏缺血再灌注时中性粒细胞的聚集。
J Pharmacol Exp Ther. 1998 Mar;284(3):1139-46.
5
Acute lung injury: the role of cytokines in the elicitation of neutrophils.急性肺损伤:细胞因子在中性粒细胞募集过程中的作用
J Investig Med. 1994 Dec;42(4):640-51.
6
Pulmonary microvascular injury following intestinal reperfusion.肠道再灌注后的肺微血管损伤。
New Horiz. 1994 Nov;2(4):463-75.
7
The inflammatory response to cardiopulmonary bypass and its impact on postoperative myocardial function.体外循环的炎症反应及其对术后心肌功能的影响。
Curr Opin Cardiol. 1995 Nov;10(6):597-604.
8
Peroxynitrite is an important mediator in thermal injury-induced lung damage.过氧亚硝酸盐是热损伤诱导的肺损伤中的一种重要介质。
Crit Care Med. 2003 Aug;31(8):2170-7. doi: 10.1097/01.CCM.0000079605.28852.D0.
9
Neutrophil oxygen radical generation. Synergistic responses to tumor necrosis factor and mono/polyunsaturated fatty acids.中性粒细胞氧自由基生成。对肿瘤坏死因子和单/多不饱和脂肪酸的协同反应。
J Clin Invest. 1996 Apr 1;97(7):1605-9. doi: 10.1172/JCI118585.
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The role of reactive nitrogen/oxygen intermediates in cytokine-induced trophoblast apoptosis.
Placenta. 1999 May;20(4):309-15. doi: 10.1053/plac.1998.0383.

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