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Cellular changes in bronchoalveolar lavage fluid in hyperoxia-induced lung injury

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Abstract

It is well known that high concentration oxygen exposure is a model of acute lung injury (ALI). However, controversy exists over the mechanism. This study was designed to clarify the cellular characteristics in bronchoalveolar lavage fluid (BALF) and body weight loss of rats exposed to oxygen(> 90%). Young male Wistar rats, aged 6 weeks, were divided into three groups: (1) room air group (exposed to room air, n = 22); (2) hyperoxia < 48 h group (exposed to over 90% oxygen for less than 48 h, n = 18); (3) hyperoxia 66–72 h group (exposed to over 90% oxygen for 66–72 h group, n = 7). Compared to the room air group, the total cell counts in the hyperoxia 66–72 h group decreased, whereas the neutrophils increased significantly. The body weights of the rats exposed to room air continued to increase. However, the body weights of oxygen-exposed rats increased slightly on the first day and weight loss was seen from the second day. All rats were noted to have bilateral pleural effusion in the hyperoxia 66–72 h group. The data suggests that (1) an increase in neutrophil count is an evident feature of hyperoxia-induced lung injury; (2) high concentration oxygen exposure can give rise to anorexia and malnutrition, which may play a role in hyperoxia-induced lung injury. Blocking neutrophil influx into lung tissue in the early phase and improving malnutrition are two effective methods to reduce hyperoxic lung injury.

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Authors and Affiliations

  1. Department of Emergency, The Second Hospital, Tianjin Medical University, Tianjin, 300211, China

    Xinbiao He

  2. Institute of Public Health, Tianjin Medical University, Tianjin, 300070, China

    Wei Zhao

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  1. Xinbiao He
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  2. Wei Zhao
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Correspondence to Xinbiao He.

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He, X., Zhao, W. Cellular changes in bronchoalveolar lavage fluid in hyperoxia-induced lung injury. Front. Med. China 2, 370–373 (2008). https://doi.org/10.1007/s11684-008-0071-5

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  • DOI: https://doi.org/10.1007/s11684-008-0071-5

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