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[高氧诱导的肺毒性]

[Hyperoxia-induced pulmonary toxicity].

作者信息

Gordo-Vidal F, Calvo-Herranz E, Abella-Alvarez A, Salinas-Gabiña I

机构信息

Servicio de Medicina Intensiva, Hospital del Henares, Coslada, Madrid, España.

出版信息

Med Intensiva. 2010 Mar;34(2):134-8. doi: 10.1016/j.medin.2009.04.007. Epub 2009 Sep 24.

Abstract

Mechanical ventilation may cause and aggravate lung damage and contribute to the appearance of multiorgan failure. One of the mechanisms that has been described is alveolar hyperoxia. In experimental models, it has lead to the production of free oxygen radicals that exceed the cell defense capacity, giving rise to inflammation, cell damage and gene overexpression with necrosis and apoptosis phenomenon. However, these findings in humans are not as conclusive, although a functional alteration due to the exposure to high FiO(2), and greater lung de-recruitment in patients with lung injury has been clearly demonstrated. Moreover, both the FiO(2) used as well as the PaO(2) achieved in the first 24h of admission are associated with mortality. Clinical trials are needed that assess the threshold of the safe oxygen level for FiO(2) and oxygen saturation.

摘要

机械通气可能会导致并加重肺损伤,促使多器官功能衰竭的出现。已被描述的机制之一是肺泡高氧。在实验模型中,它会导致产生超过细胞防御能力的游离氧自由基,引发炎症、细胞损伤以及伴有坏死和凋亡现象的基因过度表达。然而,尽管已明确证实在人类中暴露于高吸入氧分数(FiO₂)会导致功能改变,且肺损伤患者的肺复张程度更低,但这些发现并不那么确凿。此外,入院后首个24小时内使用的FiO₂以及所达到的动脉血氧分压(PaO₂)均与死亡率相关。需要开展临床试验来评估FiO₂和氧饱和度的安全氧水平阈值。

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