کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2847343 1167353 2012 7 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
In vivo and in vitro lung mechanics by forced oscillations: Effect of bleomycin challenge
موضوعات مرتبط
علوم زیستی و بیوفناوری بیوشیمی، ژنتیک و زیست شناسی مولکولی فیزیولوژی
پیش نمایش صفحه اول مقاله
In vivo and in vitro lung mechanics by forced oscillations: Effect of bleomycin challenge
چکیده انگلیسی

Bleomycin injury causes biomechanical changes secondary to inflammation, tissue remodeling and surfactant changes. We compared lung mechanics in open chest (OC) and tissue strip (TS) to better understand the pathophysiology of the alveolar interface between lung tissue and conducting airways. Thirty nine rats were studied at days 3, 7, and 15 after receiving saline or bleomycin (2.5 U kg−1) intratracheally. Normalized elastance (E), hysteresivity (η) and exponent (β) of the power frequency dependence of elastance were determined in OC (lung parenchyma) and TS. Remodeling (hydroxyproline) and inflammation (myeloperoxidase and lung water) parameters were determined. E, η and β were higher in OC both in saline and bleomycin groups. The difference (OC-TS) of η and β correlated with myeloperoxidase and lung water but not with hydroxyproline. We concluded that differences between lung parenchyma and tissue mechanics are due to mechanical effects of inhomogeneities in saline animals. Changes at the alveolar interface after bleomycin are related to oxidative stress and extravascular lung water.


► We compared lung mechanics in open chest (OC) and tissue strip (TS) to understand the pathophysiology of the alveolar interface between lung tissue and conducting airways after bleomycin challenge.
► Hysteresivity (η), exponent (β) of the frequency dependence of elastance, hydroxyproline, myeloperoxidase and lung water were determined.
► The difference (OC-TS) of η and β correlated with myeloperoxidase and lung water but not with hydroxyproline.
► Changes at the alveolar interface after bleomycin are related to inflammation and alveolar epithelium damage.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Respiratory Physiology & Neurobiology - Volume 181, Issue 1, 15 April 2012, Pages 46–52
نویسندگان
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