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自主神经系统功能衰竭在危及生命的特发性系统性毛细血管渗漏综合征中的作用

The Role of Failing Autonomic Nervous System on Life-Threatening Idiopathic Systemic Capillary Leak Syndrome.

作者信息

Colombo Riccardo, Wu Maddalena Alessandra, Catena Emanuele, Perotti Andrea, Fossali Tommaso, Cioffi Federico, Rech Roberto, Castelli Antonio, Cicardi Marco

机构信息

Department of Anesthesiology and Intensive Care, ASST Fatebenefratelli Sacco, Luigi Sacco Hospital - Polo ospedaliero, University of Milan, Milan, Italy.

Department of Biomedical and Clinical Sciences, ASST Fatebenefratelli Sacco, Luigi Sacco Hospital - Polo ospedaliero, University of Milan, Milan, Italy.

出版信息

Front Med (Lausanne). 2018 Apr 20;5:111. doi: 10.3389/fmed.2018.00111. eCollection 2018.

DOI:10.3389/fmed.2018.00111
PMID:29732372
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5919959/
Abstract

Idiopathic systemic capillary leak syndrome (ISCLS) is a rare disease that involves the endothelium and microcirculation, leading to an abrupt shift of fluids and proteins from the intravascular to the interstitial compartment. The consequence of the capillary leakage is a life-threatening hypovolemic shock that can lead to lethal multiple organ dysfunction. The autonomic nervous system (ANS) is central in regulating the cardiovascular response to hypovolemia, but ANS modulation in ISCLS has not yet been investigated. Here, we report ANS activity during acute phase and recovery from a severe ISCLS shock and speculate on the possibility that autonomic mechanisms underlie the pathogenesis of attacks.

摘要

特发性系统性毛细血管渗漏综合征(ISCLS)是一种罕见疾病,累及内皮和微循环,导致液体和蛋白质从血管内突然转移至间质腔隙。毛细血管渗漏的后果是危及生命的低血容量性休克,可导致致命的多器官功能障碍。自主神经系统(ANS)在调节心血管系统对低血容量的反应中起核心作用,但ISCLS中ANS的调节作用尚未得到研究。在此,我们报告了严重ISCLS休克急性期和恢复过程中的ANS活动,并推测自主机制可能是发作性疾病发病机制的基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a92/5919959/146decd2ab07/fmed-05-00111-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a92/5919959/3e98c6c240c8/fmed-05-00111-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a92/5919959/146decd2ab07/fmed-05-00111-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a92/5919959/3e98c6c240c8/fmed-05-00111-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2a92/5919959/146decd2ab07/fmed-05-00111-g002.jpg

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