自主神经系统功能障碍及其在感染性危重疾病发病机制中的作用(综述)。

IF 1.1 Q4 MEDICINE, RESEARCH & EXPERIMENTAL Sovremennye Tehnologii v Medicine Pub Date : 2021-01-01 Epub Date: 2020-08-27 DOI:10.17691/stm2020.12.4.12
Y Y Kiryachkov, S A Bosenko, B G Muslimov, M V Petrova
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引用次数: 1

摘要

在败血症中,大脑自主神经系统(ANS)的功能障碍可引起严重的全身性炎症甚至死亡。大量数据证实了ANS功能障碍在全身性败血症的发生、过程和结果中的作用。ANS的副交感神经部分通过内脏器官、巨噬细胞和淋巴细胞的胆碱能受体(胆碱能抗炎途径)改变炎症。ANS的交感神经部分通过影响β2-肾上腺素能受体来控制巨噬细胞和淋巴细胞的活性,引起细胞内编码细胞因子合成的基因(抗炎β2-肾上腺素能受体白介素-10通路,β2AR-IL-10)的激活。ANS与感染因子和免疫系统的相互作用确保维持体内平衡或出现严重的全身性感染。炎症时,ANS通过释放交感或副交感神经递质和神经肽参与炎症反应。在危急情况下,确定ANS的功能状态是非常重要的,因为胆碱能和拟交感神经药物都可以作为抗炎或促炎刺激。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Dysfunction of the Autonomic Nervous System and its Role in the Pathogenesis of Septic Critical Illness (Review).

Dysfunction of the autonomic nervous system (ANS) of the brain in sepsis can cause severe systemic inflammation and even death. Numerous data confirmed the role of ANS dysfunction in the occurrence, course, and outcome of systemic sepsis. The parasympathetic part of the ANS modifies the inflammation through cholinergic receptors of internal organs, macrophages, and lymphocytes (the cholinergic anti-inflammatory pathway). The sympathetic part of ANS controls the activity of macrophages and lymphocytes by influencing β2-adrenergic receptors, causing the activation of intracellular genes encoding the synthesis of cytokines (anti-inflammatory beta2-adrenergic receptor interleukin-10 pathway, β2AR-IL-10). The interaction of ANS with infectious agents and the immune system ensures the maintenance of homeostasis or the appearance of a critical generalized infection. During inflammation, the ANS participates in the inflammatory response by releasing sympathetic or parasympathetic neurotransmitters and neuropeptides. It is extremely important to determine the functional state of the ANS in critical conditions, since both cholinergic and sympathomimetic agents can act as either anti- or pro-inflammatory stimuli.

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来源期刊
Sovremennye Tehnologii v Medicine
Sovremennye Tehnologii v Medicine MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
1.80
自引率
0.00%
发文量
38
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