ArticleJournal of toxicologic pathology2013
Pulmonary edema due to oral gavage in a toxicological study related to aquaporin-1, -4 and -5 expression.
Article in Journal of toxicologic pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Dai-Huang-Fu-Zi-Tang alleviates pulmonary and intestinal injury with severe acute pancreatitis via regulating aquaporins in rats.BMC complementary and alternative medicine · 2017Article
- Tight junctions in pulmonary epithelia during lung inflammation.Pflugers Archiv : European journal of physiology · 2017Review
- Article
- Pulmonary epithelial barrier function: some new players and mechanisms.American journal of physiology. Lung cellular and molecular physiology · 2015Review
- Chronic ingestion of high dosed Phikud Navakot extraction induces mesangiolysis in rats with alteration of AQP1 and Hsp60 expressions.BioMed research international · 2015Article
- Thaliporphine derivative improves acute lung injury after traumatic brain injury.BioMed research international · 2015Article
- Aquaporins in lung health and disease: Emerging roles, regulation, and clinical implications.Respiratory medicineReview
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A one-time oral gavage can be enough to cause of alveologenic edema with higher expression of AQP-1 and -4 than that with repeated-dose oral gavage, which caused both profound perivascular edema and hydrostatic pressure edema, while AQP-5 was similarly expressed. The alteration of AQPs expression was probably related to alveolar fluid clearance across the alveolar and bronchiolar epithelium in different stages of lung injury. The results clarified the type of lung edema in acute and sub-chronic toxicity studies without treatment related effect of tested material. The pathogenesis of pulmonary edema due to oral gavage toxicological study is associated with the cellular immune response to the reflux materials. Mast cell and leukocyte accumulation may contribute to increase vascular permeability leading to permeability edema. The increase in alveolar septum epithelium, perivascular and peribronchial cuffing, accumulation alveolar lipid containing macrophage and medial hyperplasia of the pulmonary artery might have been caused to increase airway resistance, which resulted in hydrostatic pressure edema.
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