Journal Information
Vol. 89. Issue 3.
Pages 300-306 (May - June 2013)
Share
Share
Download PDF
More article options
Vol. 89. Issue 3.
Pages 300-306 (May - June 2013)
ARTIGO ORIGINAL
Open Access
Alterations in the pulmonary histoarchitecture of neonatal mice exposed to hyperoxia
Alterações da histoarquitetura pulmonar de camundongos neonatos expostos à hiperóxia
Visits
4734
Renata B. Reisa, Akinori C. Nagatob, Clarissa R. Nardelic, Isadora C.P. Matiasc, Wanderson G. Limad, Frank S. Bezerrae,
Corresponding author
frank@iceb.ufop.br

Corresponding author.
a Acadêmica. Curso de Fisioterapia, Laboratório de Biomorfologia e Patologia Experimental, Centro de Ciências da Saúde, Universidade Severino Sombra (USS), Vassouras, RJ, Brasil
b Mestre em Ciências. Professor-assistente, Laboratório de Biomorfologia e Patologia Experimental, Centro de Ciências da Saúde, USS, Vassouras, RJ, Brasil
c Acadêmica. Curso de Biomedicina, Laboratório de Biomorfologia e Patologia Experimental, Centro de Ciências da Saúde, USS, Vassouras, RJ, Brasil
d Doutor em Patologia. Professor Adjunto, Laboratório de Imunopatologia, Departamento de Ciências Biológicas, Universidade Federal de Ouro Preto (UFOP), Ouro Preto, MG, Brasil
e Doutor em Ciências Morfológicas. Professor Adjunto, Laboratório de Medicina Metabólica, Departamento de Ciências Biológicas, UFOP, Ouro Preto, MG, Brasil
Related content
Renata B. Reis, Akinori C. Nagato, Clarissa R. Nardeli, Isadora C.P. Matias, Wanderson G. Lima, Frank S. Bezerra
J Pediatr (Rio J). 2013;89:514-510.1016/j.jpedp.2013.07.003
Shruti Shree Joshi, Arpita Kalla Vyas, Dinesh Vyas, Rahul Kalla
This item has received

Under a Creative Commons license
Article information
Abstract
Objectives

To analyze the effects of exposure to hyperoxia (100% oxygen) on the lung histoarchitecture of neonatal mice.

Methods

Neonatal Balb/c mice were exposed to hyperoxia (HG) (100% oxygen) (n = 10) in a chamber (15 x 20 x 30cm) for 24hours with a flow of 2 L/min. The control group (CG) (n = 10) was exposed to normoxia in the same type of chamber and for the same time. After exposure, the animals were euthanized by decapitation; the lungs were removed and processed for histological examination according to the laboratory routine. Three-mm thick sections were stained with hematoxylin and eosin (H&E). The morphometric analysis was performed with in order to analyze the macrophages present in the alveolar lumen, surface density (Sv) of gas exchange, volume density (Vv) of lung parenchyma, and areas of atelectasis.

Results

A decrease in the number of alveolar macrophages (MØ) was observed in the HG (HG = 0.08±0.01 MØ/mm2, CG = 0.18±0.03 MØ/mm2, p = 0.0475), Sv of gas exchange in HG (HG = 8.08±0.12 mm2/mm3, CG=8.65±0.20 mm2/mm3, p=0.0233), Vv of lung parenchyma in HG (HG=54.7/33.5/83.5%/ mm2; CG=75/56.7/107.9%/mm2, p<0.0001) when compared with the CG. However, there was an increase in areas of atelectasis in HG (HG=17.5/11.3/38.4 atelectasis/mm2, CG=14/6.1/24.4 atelectasis/mm2, p=0.0166) when compared with the CG.

Conclusion

The present results indicate that hyperoxia caused alterations in lung histoarchitecture, increasing areas of atelectasis and diffuse alveolar hemorrhage.

Keywords:
Hyperoxia
Lung
Newborn animals
Resumo
Objetivos

Analisar os efeitos da exposição à hiperóxia (100% de oxigênio) sobre a his- toarquitetura pulmonar de camundongos neonatos.

Métodos

Camundongos neonatos da linhagem Balb/c foram expostos à hiperóxia (GH) (100% de oxigênio) (n=10) em uma câmara (15×20×30cm) por 24h, com fluxo de 2 L/ min. O grupo controle (GC) (n=10) foi exposto a normóxia em um mesmo tipo de câmara e pelo mesmo tempo. Após a exposição, os animais foram sacrificados por decapitação, os pulmões foram removidos para análise histológica e processados de acordo com a rotina do laboratório. Cortes de 3μm de espessura foram corados com hematoxilina e eosina (H&E). A análise morfométrica foi realizada com o objetivo de analisar macrófa- gos presentes na luz alveolar, densidade de superfície (Sv) de trocas gasosas, densidade de volume (Vv) de parênquima pulmonar e áreas de atelectasias.

Resultados

Foi verificada diminuição do número de macrófagos alveolares (MØ) no GH (GH=0,08±0,01 MØ/mm2; GC=0,18±0,03 MØ/mm2; p=0,0475), Sv de troca gasosa no GH (GH=8,08±0,12 mm2/mm3; GC=8,65±0,20 mm2/mm3; p=0,0233), Vv de parên- quima pulmonar no GH (GH=54,7/33,5/83,5%/mm2; GC=75/56,7/107,9%/mm2; p<0.0001) quando comparado com o GC. Entretanto, houve aumento de áreas de atelecta- sias no GH (GH=17,5/11,3/38,4 atelectasia/mm2; GC=14/6,1/24,4 atelectasia/mm2; p=0,0166) quando comparado com o GC.

Conclusão

Nossos resultados indicam que a hiperóxia promoveu alterações na histoar- quitetura pulmonar, aumentando áreas de atelectasia e hemorragia alveolar difusa.

Palavras chave:
Hiperóxia
Pulmão
Animais recém- nascidos
Full text is only aviable in PDF
Referências
[1]
T. Duke.
Neonatal pneumonia in developing countries.
Arch Dis Child Fetal Neonatal Ed, 90 (2005), pp. F211-F219
[2]
B. Frey, F. Shann.
Oxygen administration in infants.
Arch Dis Child Fetal Neonatal Ed, 88 (2003), pp. F84-F88
[3]
T. Duke, S.M. Graham, M.N. Cherian, A.S. Ginsburg, M. English, S. Howie, et al.
Oxygen is an essential medicine: a call for international action.
Int J Tuberc Lung Dis., 14 (2010), pp. 1362-1368
[4]
M.A. O’Reilly.
DNA damage and cell cycle checkpoints in hyperoxic lung injury: braking to facilitate repair.
Am J Physiol Lung Cell Mol Physiol., 281 (2001), pp. L291-L305
[5]
S. Usen, M. Webert.
Clinical signs of hypoxaemia in children with acute lower respiratory infection: indicators of oxygen therapy.
Int J Tuberc Lung Dis., 5 (2001), pp. 505-510
[6]
H. Reissmann, S.H. Böhm, F. Suárez-Sipmann, G. Tusman, C. Buschmann, S. Maisch, et al.
Suctioning through a double-lumen endotracheal tube helps to prevent alveolar collapse and to preserve ventilation.
Intensive Care Med., 31 (2005), pp. 431-440
[7]
W.W. Hay Jr., E.F. Bell.
Oxygen therapy, oxygen toxicity, and the STOP-ROP trial.
Pediatrics., 105 (2000), pp. 424-425
[8]
Y. Kim, H. Kim, H.Y. Yoo, J.S. Kang, S.J. Kim, J.K. Kim, et al.
Suppression of CFTR-mediated Cl secretion of airway epithelium in vitamin C-deficient mice.
J Korean Med Sci., 26 (2011), pp. 317-324
[9]
T. Minamino, I. Komuro.
Regeneration of the endothelium as a novel therapeutic strategy for acute lung injury.
J Clin Invest., 116 (2006), pp. 2316-2319
[10]
A.C. Nagato, F.S. Bezerra, M. Lanzetti, A.A. Lopes, M.A. Silva, L.C. Porto, et al.
Time course of inflammation, oxidative stress and tissue damage induced by hyperoxia in mouse lungs.
Int J Exp Pathol., 93 (2012), pp. 269-278
[11]
C.A. Mandarim-de-Lacerda.
Stereological tools in biomedical research.
An Acad Bras Cienc., 75 (2003), pp. 469-486
[12]
I. Petrache, M.E. Choi, L.E. Otterbein, B.Y. Chin, L.L. Mantell, S. Horowitz, et al.
Mitogen-activated protein kinase pathway mediates hyperoxia-induced apoptosis in cultured macrophage cells.
Am J Physiol., 277 (1999), pp. L589-L595
[13]
T. Nyunoya, M.M. Monick, L.S. Powers, T.O. Yarovinsky, G.W. Hunninghake.
Macrophages survive hyperoxia via prolonged ERK activation due to phosphatase down-regulation.
J Biol Chem., 280 (2005), pp. 26295-26302
[14]
P.J. O’Reilly, J.M. Hickman-Davis, I.C. Davis, S. Matalon.
Hyperoxia impairs antibacterial function of macrophages through effects on actin.
Am J Respir Cell Mol Biol., 28 (2003), pp. 443-450
[15]
B. Thébaud, F. Ladha, E.D. Michelakis, M. Sawicka, G. Thurston, F. Eaton, et al.
Vascular endothelial growth factor gene therapy increases survival, promotes lung angiogenesis, and prevents alveolar damage in hyperoxia-induced lung injury: evidence that angiogenesis participates in alveolarization.
Circulation., 112 (2005), pp. 2477-2486
[16]
R.S. Mascaretti, M.M. Mataloun, M. Dolhnikoff, C.M. Rebello.
Lung morphometry, collagen and elastin content: changes after hyperoxic exposure in preterm rabbits.
Clinics (São Paulo), 64 (2009), pp. 1099-1104
[17]
J.R. Wispe, R.J. Roberts.
Molecular basis of pulmonary oxygen toxicity.
Clin Perinatol., 14 (1987), pp. 651-666
[18]
J.D. Crapo.
Morphologic changes in pulmonary oxygen toxicity.
Annu Rev Physiol., 48 (1986), pp. 721-731
[19]
L.F. Monte, L.V. Silva Filho, M.H. Miyoshi, T. Rozov.
Displasia broncopulmonar.
J Pediatr (Rio J)., 81 (2005), pp. 99-110
[20]
S. Dauger, L. Ferkdadji, G. Saumon, G. Vardon, M. Peuchmaur, C. Gaultier, et al.
Neonatal exposure to 65% oxygen durably impairs lung architecture and breathing pattern in adult mice.
Chest., 123 (2003), pp. 530-538
[21]
L.K. Rogers, T.E. Tipple, L.D. Nelin, S.E. Welty.
Differential responses in the lungs of newborn mouse pups exposed to 85% or >95% oxygen.
Pediatr Res., 65 (2009), pp. 33-38
[22]
C.R. Carvalho, G. de Paula Pinto Schettino, B. Maranhão, E.P. Bethlem.
Hyperoxia and lung disease.
Curr Opin Pulm Med., 4 (1998), pp. 300-304
[23]
G.M. Loewen, B.A. Holm, L. Milanowski, L.M. Wild, R.H. Notter, S. Matalon.
Alveolar hyperoxic injury in rabbits receiving exogenous surfactant.
J Appl Physiol., 66 (1989), pp. 1087-1092
[24]
G. Buonocore, S. Perrone, M.L. Tataranno.
Oxygen toxicity: chemistry and biology of reactive oxygen species.
Semin Fetal Neonatal Med., 15 (2010), pp. 186-190
[25]
M. Yamada, H. Kubo, S. Kobayashi, K. Ishizawa, H. Sasaki, Interferon-gamma:.
a key contributor to hyperoxia-induced lung injury in mice.
Am J Physiol Lung Cell Mol Physiol., 287 (2004), pp. L1042-L1047
[26]
K. Tokieda, H.S. Iwamoto, C. Bachurski, S.E. Wert, W.M. Hull, K. Ikeda, et al.
Surfactant protein-B-deficient mice are susceptible to hyperoxic lung injury.
Am J Respir Cell Mol Biol., 21 (1999), pp. 463-472
[27]
X. Lian, Y. Qin, S.A. Hossain, L. Yang, A. White, H. Xu, et al.
Overexpression of Stat3C in pulmonary epithelium protects against hyperoxic lung injury.
J Immunol., 174 (2005), pp. 7250-7256
[28]
Y. Song, N. Fukuda, C. Bai, T. Ma, M.A. Matthay, A.S. Verkman.
Role of aquaporins in alveolar fluid clearance in neonatal and adult lung, and in oedema formation following acute lung injury: studies in transgenic aquaporin null mice.
J Physiol., 525 (2000), pp. 771-779
[29]
P.B. Babu, A. Chidekel, T.H. Shaffer.
Hyperoxia-induced changes in human airway epithelial cells: the protective effect of perflubron.
Pediatr Crit Care Med., 6 (2005), pp. 188-194
[30]
P. Minoo, R.J. King.
Epithelial-mesenchymal interactions in lung development.
Annu Rev Physiol., 56 (1994), pp. 13-45

Como citar este artigo: Reis RB, Nagato AC, Nardeli CR, Matias IC, Lima WG, Bezerra FS. Alterations in the pulmonary histoarchitecture of neonatal mice exposed to hyperoxia. J Pediatr (Rio J). 2013;89:300–6.

Copyright © 2013. Sociedade Brasileira de Pediatria
Download PDF
Idiomas
Jornal de Pediatria (English Edition)
Article options
Tools
en pt
Taxa de publicaçao Publication fee
Os artigos submetidos a partir de 1º de setembro de 2018, que forem aceitos para publicação no Jornal de Pediatria, estarão sujeitos a uma taxa para que tenham sua publicação garantida. O artigo aceito somente será publicado após a comprovação do pagamento da taxa de publicação. Ao submeterem o manuscrito a este jornal, os autores concordam com esses termos. A submissão dos manuscritos continua gratuita. Para mais informações, contate assessoria@jped.com.br. Articles submitted as of September 1, 2018, which are accepted for publication in the Jornal de Pediatria, will be subject to a fee to have their publication guaranteed. The accepted article will only be published after proof of the publication fee payment. By submitting the manuscript to this journal, the authors agree to these terms. Manuscript submission remains free of charge. For more information, contact assessoria@jped.com.br.
Cookies policy Política de cookies
To improve our services and products, we use "cookies" (own or third parties authorized) to show advertising related to client preferences through the analyses of navigation customer behavior. Continuing navigation will be considered as acceptance of this use. You can change the settings or obtain more information by clicking here. Utilizamos cookies próprios e de terceiros para melhorar nossos serviços e mostrar publicidade relacionada às suas preferências, analisando seus hábitos de navegação. Se continuar a navegar, consideramos que aceita o seu uso. Você pode alterar a configuração ou obter mais informações aqui.