Hyperventilation worsens inflammatory lung injury in spontaneously breathing rats.

IF 2.9 4区医学 Q2 RESPIRATORY SYSTEM

Jornal Brasileiro De Pneumologia Pub Date : 2024-12-16 eCollection Date: 2024-01-01 DOI:10.36416/1806-3756/e20240269

Juliana Dias Nascimento Ferreira, Maycon Moura Reboredo, Eduardo Leite Vieira Costa, Lídia Maria Carneiro da Fonseca, Jaime Retamal, Fabrício Júnio Mendes Santos, Flavia de Paoli, Adenilson de Souza da Fonseca, Leda Marília Fonseca Lucinda, Bruno Valle Pinheiro

{"title":"Hyperventilation worsens inflammatory lung injury in spontaneously breathing rats.","authors":"Juliana Dias Nascimento Ferreira, Maycon Moura Reboredo, Eduardo Leite Vieira Costa, Lídia Maria Carneiro da Fonseca, Jaime Retamal, Fabrício Júnio Mendes Santos, Flavia de Paoli, Adenilson de Souza da Fonseca, Leda Marília Fonseca Lucinda, Bruno Valle Pinheiro","doi":"10.36416/1806-3756/e20240269","DOIUrl":null,"url":null,"abstract":"Objectives: Here, we investigated the effects of hyperventilation on acute lung injury (ALI) in spontaneously breathing rats.Methods: Wistar rats were randomized to receive either intraperitoneal lipopolysaccharides (LPS) or saline, and intravenous infusion of NH4Cl (to induce metabolic acidosis and hyperventilation) or saline. Four groups were established: control-control (C-C), control-hyperventilation (C-HV), LPS-control (LPS-C), and LPS-hyperventilation (LPS-HV). Venous blood gases were collected before and after NH4Cl infusion and analyzed to confirm the presence of metabolic acidosis and hyperventilation. After euthanasia, lung injury was assessed using the ALI score, morphometric quantification of perivascular edema, neutrophil counts in the bronchoalveolar lavage, and mRNA expression of biological markers in the lung tissue.Results: Hyperventilation induced inflammatory lung injury in previously healthy lungs and exacerbated injuries previously induced by LPS (ALI score: C-C=0.14 [IQR 0.12; 0.14]; C-HV=0.36 [IQR 0.31; 0.37]; LPS-C=0.51 [IQR 0.50; 0.54]; LPS-HV=0.58 [IQR 0.56; 0.62]; p<0.01). Perivascular edema, neutrophil counts in bronchoalveolar lavage, and amphiregulin mRNA expression were higher in the LPS-HV group compared to the control group.Conclusions: Hyperventilation increased inflammatory injury in rats with ALI during spontaneous ventilation. These results suggest that the impact of vigorous spontaneous breathing efforts on worsening inflammatory lung injury warrants further investigation.","PeriodicalId":14845,"journal":{"name":"Jornal Brasileiro De Pneumologia","volume":"50 6","pages":"e20240269"},"PeriodicalIF":2.9000,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11601074/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Jornal Brasileiro De Pneumologia","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.36416/1806-3756/e20240269","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"RESPIRATORY SYSTEM","Score":null,"Total":0}

引用次数: 0

Abstract

Objectives: Here, we investigated the effects of hyperventilation on acute lung injury (ALI) in spontaneously breathing rats.

Methods: Wistar rats were randomized to receive either intraperitoneal lipopolysaccharides (LPS) or saline, and intravenous infusion of NH4Cl (to induce metabolic acidosis and hyperventilation) or saline. Four groups were established: control-control (C-C), control-hyperventilation (C-HV), LPS-control (LPS-C), and LPS-hyperventilation (LPS-HV). Venous blood gases were collected before and after NH4Cl infusion and analyzed to confirm the presence of metabolic acidosis and hyperventilation. After euthanasia, lung injury was assessed using the ALI score, morphometric quantification of perivascular edema, neutrophil counts in the bronchoalveolar lavage, and mRNA expression of biological markers in the lung tissue.

Results: Hyperventilation induced inflammatory lung injury in previously healthy lungs and exacerbated injuries previously induced by LPS (ALI score: C-C=0.14 [IQR 0.12; 0.14]; C-HV=0.36 [IQR 0.31; 0.37]; LPS-C=0.51 [IQR 0.50; 0.54]; LPS-HV=0.58 [IQR 0.56; 0.62]; p<0.01). Perivascular edema, neutrophil counts in bronchoalveolar lavage, and amphiregulin mRNA expression were higher in the LPS-HV group compared to the control group.

Conclusions: Hyperventilation increased inflammatory injury in rats with ALI during spontaneous ventilation. These results suggest that the impact of vigorous spontaneous breathing efforts on worsening inflammatory lung injury warrants further investigation.

查看原文本刊更多论文

过度换气加重自主呼吸大鼠炎性肺损伤。

目的：研究过度通气对自主呼吸大鼠急性肺损伤（ALI）的影响。方法：Wistar大鼠随机分为两组：腹腔注射脂多糖（LPS）或生理盐水，静脉输注NH4Cl（诱导代谢性酸中毒和过度通气）或生理盐水。建立4组：对照组-对照组（C-C）、对照组-过度通气（C-HV）、lps -对照组（LPS-C）和lps -过度通气（LPS-HV）。在输注NH4Cl前后采集静脉血气体，分析是否存在代谢性酸中毒和换气过度。安乐死后，采用ALI评分、血管周围水肿形态学量化、支气管肺泡灌洗液中性粒细胞计数和肺组织生物标志物mRNA表达来评估肺损伤。结果：过度换气诱导原健康肺炎性肺损伤，并加重原LPS诱导的肺损伤(ALI评分：C-C=0.14 [IQR = 0.12；0.14);C-hv =0.36 [iqr = 0.31；0.37);lp - c =0.51 [iqr = 0.50；0.54);lp - hv =0.58 [iqr = 0.56；0.62);结论：过度通气增加了ALI大鼠自发通气时的炎症损伤。这些结果表明，剧烈自主呼吸对炎症性肺损伤恶化的影响值得进一步研究。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Jornal Brasileiro De Pneumologia RESPIRATORY SYSTEM-

CiteScore

3.50

自引率

14.80%

发文量

118

审稿时长

20 weeks

期刊介绍： The Brazilian Journal of Pulmonology publishes scientific articles that contribute to the improvement of knowledge in the field of the lung diseases and related areas.