Neonatal lungs-can absolute lung resistivity be determined non-invasively?

2002 ◽  
Vol 40 (4) ◽  
pp. 388-394 ◽  
Author(s):  
B. H. Brown ◽  
R. A. Primhak ◽  
R. H. Smallwood ◽  
P. Milnes ◽  
A. J. Narracott ◽  
...  
2002 ◽  
Vol 40 (5) ◽  
pp. 506-511 ◽  
Author(s):  
B. H. Brown ◽  
R. A. Primhak ◽  
R. H. Smallwood ◽  
P. Milnes ◽  
A. J. Narracott ◽  
...  

2007 ◽  
Vol 29 (1) ◽  
pp. 93-100 ◽  
Author(s):  
S. Zlochiver ◽  
M. Arad ◽  
M.M. Radai ◽  
D. Barak-Shinar ◽  
H. Krief ◽  
...  

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1874
Author(s):  
Hye-Youn Cho ◽  
Laura Miller-DeGraff ◽  
Ligon A. Perrow ◽  
Wesley Gladwell ◽  
Vijayalakshmi Panduri ◽  
...  

NRF2 protects against oxidant-associated airway disorders via cytoprotective gene induction. To examine if NRF2 is an important determinant of respiratory syncytial virus (RSV) susceptibility after neonate lung injury, Nrf2-deficient (Nrf2−/−) and wild-type (Nrf2+/+) mice neonatally exposed to hyperoxia were infected with RSV. To investigate the prenatal antioxidant effect on neonatal oxidative lung injury, time-pregnant Nrf2−/−and Nrf2+/+mice were given an oral NRF2 agonist (sulforaphane) on embryonic days 11.5–17.5, and offspring were exposed to hyperoxia. Bronchoalveolar lavage and histopathologic analyses determined lung injury. cDNA microarray analyses were performed on placenta and neonatal lungs. RSV-induced pulmonary inflammation, injury, oxidation, and virus load were heightened in hyperoxia-exposed mice, and injury was more severe in hyperoxia-susceptible Nrf2−/− mice than in Nrf2+/+ mice. Maternal sulforaphane significantly alleviated hyperoxic lung injury in both neonate genotypes with more marked attenuation of severe neutrophilia, edema, oxidation, and alveolarization arrest in Nrf2−/− mice. Prenatal sulforaphane altered different genes with similar defensive functions (e.g., inhibition of cell/perinatal death and inflammation, potentiation of angiogenesis/organ development) in both strains, indicating compensatory transcriptome changes in Nrf2−/− mice. Conclusively, oxidative injury in underdeveloped lungs NRF2-dependently predisposed RSV susceptibility. In utero sulforaphane intervention suggested NRF2-dependent and -independent pulmonary protection mechanisms against early-life oxidant injury.


Genes ◽  
2018 ◽  
Vol 9 (9) ◽  
pp. 443 ◽  
Author(s):  
Long Jin ◽  
Silu Hu ◽  
Teng Tu ◽  
Zhiqing Huang ◽  
Qianzi Tang ◽  
...  

Lung tissue plays an important role in the respiratory system of mammals after birth. Early lung development includes six key stages, of which the saccular stage spans the pre- and neonatal periods and prepares the distal lung for alveolarization and gas-exchange. However, little is known about the changes in gene expression between fetal and neonatal lungs. In this study, we performed transcriptomic analysis of messenger RNA (mRNA) and long noncoding RNA (lncRNA) expressed in the lung tissue of fetal and neonatal piglets. A total of 19,310 lncRNAs and 14,579 mRNAs were identified and substantially expressed. Furthermore, 3248 mRNAs were significantly (FDR-adjusted p value ≤ 0.05, FDR: False Discovery Rate) differentially expressed and were mainly enriched in categories related to cell proliferation, immune response, hypoxia response, and mitochondrial activation. For example, CCNA2, an important gene involved in the cell cycle and DNA replication, was upregulated in neonatal lungs. We also identified 452 significantly (FDR-adjusted p value ≤ 0.05) differentially expressed lncRNAs, which might function in cell proliferation, mitochondrial activation, and immune response, similar to the differentially expressed mRNAs. These results suggest that differentially expressed mRNAs and lncRNAs might co-regulate lung development in early postnatal pigs. Notably, the TU64359 lncRNA might promote distal lung development by up-regulating the heparin-binding epidermal growth factor-like (HB-EGF) expression. Our research provides basic lung development datasets and will accelerate clinical researches of newborn lung diseases with pig models.


2003 ◽  
Vol 284 (5) ◽  
pp. L703-L709 ◽  
Author(s):  
Zhenxing Fu ◽  
Gregory P. Heldt ◽  
John B. West

The pulmonary capillaries of neonatal lungs are potentially vulnerable to stress failure because of the complex changes in the pulmonary circulation that occur at birth. We perfusion fixed the lungs from nine anesthetized newborn rabbits at capillary transmural pressures (Ptm) of 5 ± 5, 10 ± 5, and 15 ± 5 cmH2O. Normal microscopic appearances were seen at Ptm values of 5 ± 5 and 10 ± 5 cmH2O, but massive airway edema was observed in lungs perfused at a Ptm of 15 ± 5 cmH2O. Consistent with this, no disruptions of the alveolar epithelium were observed at Ptm values of 5 ± 5 cmH2O, but mean values of 0.11 and 1.22 breaks/mm epithelium were found at Ptm of 10 ± 5 and 15 ± 5 cmH2O, respectively ( P < 0.05 for 5 ± 5 vs. 15 ± 5 cmH2O). These pressures are in striking contrast to those in the adult rabbit in which, by a similar procedure, a Ptm of 52.5 cmH2O, is required before stress failure is consistently seen. We conclude that stress failure of pulmonary capillaries in newborn rabbit lungs can occur at Ptm values of less than one-third of those that are required in adult lungs.


1984 ◽  
Vol 15 (1) ◽  
pp. 115-128 ◽  
Author(s):  
Charles W. Leffler ◽  
Robert S. Green ◽  
Randy K. Jerkins ◽  
James L. Horton ◽  
Dominic M. Desidirio ◽  
...  

2011 ◽  
Vol 16 (12) ◽  
pp. 127002 ◽  
Author(s):  
Märta Lewander ◽  
Anders Bruzelius ◽  
Sune Svanberg ◽  
Katarina Svanberg ◽  
Vineta Fellman

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