Hyperventilation worsens inflammatory lung injury in spontaneously breathing rats

Here, we investigated the effects of hyperventilation on acute lung injury (ALI) in spontaneously breathing rats. Wistar rats were randomized to receive either intraperitoneal lipopolysaccharides (LPS) or saline, and intravenous infusion of NH4Cl (to induce metabolic acidosis and hyperventilation) o...

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Veröffentlicht in:Jornal brasileiro de pneumologia 2024, Vol.50 (6), p.e20240269
Hauptverfasser: Ferreira, Juliana Dias Nascimento, Reboredo, Maycon Moura, Costa, Eduardo Leite Vieira, Fonseca, Lídia Maria Carneiro da, Retamal, Jaime, Santos, Fabrício Júnio Mendes, Paoli, Flavia de, Fonseca, Adenilson de Souza da, Lucinda, Leda Marília Fonseca, Pinheiro, Bruno Valle
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Sprache:eng
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Zusammenfassung:Here, we investigated the effects of hyperventilation on acute lung injury (ALI) in spontaneously breathing rats. 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. 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
ISSN:1806-3756
1806-3713
1806-3756
DOI:10.36416/1806-3756/e20240269