Critical Care: Critical Care: ARDS/ALI |

Losartan, a Selective Antagonist of AT1 Receptor, Attenuates Acute Lung Injury Induced by Seawater Inhalation in Rats FREE TO VIEW

Faguang Jin, PhD
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Tangdu Hospital, Fourth Military Medical University, Xi'an, China

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;149(4_S):A155. doi:10.1016/j.chest.2016.02.161
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SESSION TYPE: Original Investigation Poster

PRESENTED ON: Saturday, April 16, 2016 at 11:45 AM - 12:45 PM

PURPOSE: Losartan is a selective antagonist of Ang I type (AT1) receptor of Angiotensin II (Ang II), which is widely used as a clinical medicine for the hypertension. Furthermore losartan was shown to protect from acute lung injury (ALI) induced by lipopolysaccharides, acid aspiration, sepsis and ventilation. The aim of this research was to clarify whether Ang II participated in the inflammatory response of ALI induced by seawater inhalation, and whether losartan had the protective effects on ALI by blocking the combination of Ang II and AT1 receptor.

METHODS: The severity of lung injury was assessed by arterial blood gases, wet to dry weight ratios, histopathological changes and myeloperoxidase (MPO) activity examination, as well as ELISA assays for Ang II, Tumor Necrosis Factor-α (TNF-α), Interleukin-1β (IL-1β), and Interleukin-8 (IL-8). Besides, we also detected the expression of AT1 receptor and the phosphorylation of NF-κB.

RESULTS: The results showed that seawater inhalation could up-regulate expression of Ang II and AT1 followed by enhanced NF-κB expression. While pretreatment of losartan (especially 15 mg/kg) alleviated lung injury by inhibiting expression of NF-κB and those following inflammatory factors.

CONCLUSIONS: In conclusion, losartan could attenuate seawater inhalation induced lung injury probably through inhibiting the combination of Ang II and AT1 receptor and further affecting the NF-κB pathway.

CLINICAL IMPLICATIONS: Losartan improved seawater instillation induced lung injury. The protection effect was through inhibiting phosphorylation of NF-κB and release of inflammatory cytokines.

DISCLOSURE: The following authors have nothing to disclose: Faguang Jin





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