ArticleActa physiologica (Oxford, England)2015
Alveolar-capillary adaptation to chronic hypoxia in the fatty lung.
Article in Acta physiologica (Oxford, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Sucrose- and fat-related metabolic states influence the adaptation of the pulmonary lipid metabolism to hypoxia.Cell and tissue research · 2025Article
- When Two Pandemics Meet: Why Is Obesity Associated with Increased COVID-19 Mortality?Med (New York, N.Y.) · 2020Review
- Acclimatization of low altitude-bred deer mice ( Peromyscus maniculatus) to high altitude.Journal of applied physiology (Bethesda, Md. : 1985) · 2018Article
- Lipid phenotyping of lung epithelial lining fluid in healthy human volunteers.Metabolomics : Official journal of the Metabolomic Society · 2018Article
- Obesity and lung disease: a toxic mix.Acta physiologica (Oxford, England) · 2015Article
- The effects of genetic deletion of Macrophage migration inhibitory factor on the chronically hypoxic pulmonary circulation.Pulmonary circulationArticle
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6 authors.
Funding
Abstract
aimObese diabetic (ZDF fa/fa) rats with genetic leptin resistance suffer chronic lipotoxicity associated with age-related lung restriction and abnormal alveolar ultrastructure. We hypothesized that these abnormalities impair adaptation to ambient hypoxia.
methodsMale fa/fa and lean (+/+) ZDF rats (4-months old) were exposed to 21 or 13% O2 for 3 weeks. Lung function was measured under anaesthesia. Lung tissue was assayed for DNA damage and ultrastructure measured by morphometry.
resultsIn normoxia, lung volume, compliance and diffusing capacity were lower, while blood flow was higher in fa/fa than +/+ rats. In hypoxia, fa/fa animals lost more weight, circulating hematocrit rose higher, and lung volume failed to increase compared to +/+. In fa/fa, the hypoxia-induced increase in post-mortem lung volume was attenuated (19%) vs. +/+ (39%). Alveolar ducts were 35% smaller in normoxia but enlarged twofold more in hypoxia compared to +/+. Hypoxia induced broad increases (90-100%) in the volumes and surface areas of alveolar septal components in +/+ lungs; these increases were moderately attenuated in fa/fa lungs (58-75%), especially that of type II epithelium volume (16 vs. 61% in +/+). In fa/fa compared to +/+ lungs, oxidative DNA damage was greater with increased hypoxia induced efflux of alveolar macrophages. Harmonic mean thickness of the diffusion barrier was higher, indicating higher structural resistance to gas transfer.
conclusionChronic lipotoxicity impaired hypoxia-induced lung expansion and compensatory alveolar growth with disproportionate effect on resident alveolar progenitor cells. The moderate structural impairment was offset by physiological adaptation primarily via a higher hematocrit.
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