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Zhou T, Song WF, Shang Y, Yao SL, Matalon S. Chin. Med. J. 2018; 131(10): 1214-1219.


Department of Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham, Birmingham, AL 35294, USA.


(Copyright © 2018, Chinese Medical Association)






OBJECTIVE: Exposure to halogens, such as chlorine or bromine, results in environmental and occupational hazard to the lung and other organs. Chlorine is highly toxic by inhalation, leading to dyspnea, hypoxemia, airway obstruction, pneumonitis, pulmonary edema, and acute respiratory distress syndrome (ARDS). Although bromine is less reactive and oxidative than chlorine, inhalation also results in bronchospasm, airway hyperresponsiveness, ARDS, and even death. Both halogens have been shown to damage the systemic circulation and result in cardiac injury as well. There is no specific antidote for these injuries since the mechanisms are largely unknown. DATA SOURCES: This review was based on articles published in PubMed databases up to January, 2018, with the following keywords: "chlorine," "bromine," "lung injury," and "ARDS." STUDY SELECTION: The original articles and reviews including the topics were the primary references.

RESULTS: Based on animal studies, it is found that inhaled chlorine will form chlorine-derived oxidative products that mediate postexposure toxicity; thus, potential treatments will target the oxidative stress and inflammation induced by chlorine. Antioxidants, cAMP-elevating agents, anti-inflammatory agents, nitric oxide-modulating agents, and high-molecular-weight hyaluronan have shown promising effects in treating acute chlorine injury. Elevated free heme level is involved in acute lung injury caused by bromine inhalation. Hemopexin, a heme-scavenging protein, when administered postexposure, decreases lung injury and improves survival.

CONCLUSIONS: At present, there is an urgent need for additional research to develop specific therapies that target the basic mechanisms by which halogens damage the lungs and systemic organs.

Language: en

吸入卤素气体诱发急性肺损伤和急性呼吸窘迫综合征的机制研究和治疗进展摘要目的:卤素气体(如氯或溴),可导致环境污染和职业伤害(肺和其他器官损伤)。吸入氯气具有强烈毒性,可致呼吸困难、低氧血症、气道梗阻、肺部炎症、肺水肿和急性呼吸窘迫综合征(ARDS)。尽管溴气的反应性和氧化性弱于氯气,但吸入溴气同样导致支气管痉挛、气道高反应性、ARDS甚至死亡。卤素气体还可损伤全身循环系统并造成心脏损伤。目前其诱发损伤的机制尚不明了,临床上尚未有特异性解毒剂。 数据来源:本文综述2018年1月前收录于Pubmed数据库的相关文章,关键词如下:氯气;溴气;肺损伤;急性呼吸窘迫综合征。 研究选择:主要参考文献为相关的论著和综述。 结果:动物实验表明:氯气吸入后形成氯衍生氧化产物,导致毒性反应。因此,潜在的治疗靶点为氯气引起氧化应激和炎症反应。抗氧化剂、c-AMP调节剂、抗炎药物、一氧化氮调节剂和高分子透明质酸对急性氯损伤有治疗作用。而体内游离血红素水平升高则和吸入溴气诱发的肺损伤相关。吸入溴气后给予可清除体内血红素的血红素结合蛋白,可明显降低肺损伤和提高生存率。 结论:目前尚需要大量基础和临床研究寻找可用于治疗吸入卤素气体后诱发的肺和气体脏器损伤的特异性药物。.

Language: zh


Acute Lung Injury; Acute Respiratory Distress Syndrome; Bromine; Chlorine


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