ArticleJournal of applied physiology (Bethesda, Md. : 1985)2012
Functional and morphological assessment of early impairment of airway function in a rat model of emphysema.
Article in Journal of applied physiology (Bethesda, Md. : 1985), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Respiratory defects in theAmerican journal of physiology. Lung cellular and molecular physiology · 2020Article
- Hyperoxia-induced lung structure-function relation, vessel rarefaction, and cardiac hypertrophy in an infant rat model.Journal of translational medicine · 2019Article
- Morphometric analysis of the non-epithelial areas of mouse bronchioles through the normal aging process.American journal of translational research · 2019Article
- Histologic and biochemical alterations predict pulmonary mechanical dysfunction in aging mice with chronic lung inflammation.PLoS computational biology · 2017Article
- Comparison between Variable and Conventional Volume-Controlled Ventilation on Cardiorespiratory Parameters in Experimental Emphysema.Frontiers in physiology · 2016Article
- MRI-based measurements of aerosol deposition in the lung of healthy and elastase-treated rats.Journal of applied physiology (Bethesda, Md. : 1985) · 2014Article
- Airflow and particle deposition simulations in health and emphysema: from in vivo to in silico animal experiments.Annals of biomedical engineering · 2014Article
- Emphysema and mechanical stress-induced lung remodeling.Physiology (Bethesda, Md.) · 2013Review
- Effects of respiratory mechanics on the capnogram phases: importance of dynamic compliance of the respiratory system.Critical care (London, England) · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
The aim of this study was to evaluate airway structure-function relations in elastase-induced emphysema in rats. Sprague-Dawley rats were treated intratracheally with 50 IU porcine pancreatic elastase (PPE, n = 8) or saline (controls, n = 6). Six weeks later, lung volumes [functional residual capacity (FRC), residual volume (RV), and total lung capacity (TLC)] and low-frequency impedance parameters (Newtonian resistance, R(N); tissue damping; tissue elastance, H) were measured, and tracheal sounds were recorded during slow inflation to TLC following in vivo degassing. The lungs were fixed and stained for standard morphometry, elastin, and collagen. In the PPE group, FRC and RV were higher [4.53 ± 0.7 (SD) vs. 3.28 ± 0.45 ml; P = 0.003 and 1.06 ± 0.35 vs. 0.69 ± 0.18 ml; P = 0.036, respectively], and H was smaller in the PPE-treated rats than in the controls (1,344 ± 216 vs. 2,178 ± 305 cmH(2)O/l; P < 0.001), whereas there was no difference in R(N). The average number of crackles per inflation was similar in the two groups; however, the crackle size distributions were different and the lower knee of the pressure-volume curves was higher in the PPE group. Microscopic images revealed different alveolar size distributions but similar bronchial diameters in the two groups. The treatment caused a slight but significant decrease in the numbers of alveolar attachments, no difference in elastin and slightly increased mean level and heterogeneity of collagen in the bronchial walls. These results suggest that tissue destruction did not affect the conventionally assessed airway resistance in this emphysema model, whereas the alterations in the recruitment dynamics can be an early manifestation of impaired airway function.
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