Publication: Pulmonary Edema Due to Oral Gavage in a Toxicological Study Related to Aquaporin-1, -4 and -5 Expression
Issued Date
2015-02-27
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eng
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Mahidol University
Bibliographic Citation
Journal of Toxicologic Pathology. Vol.26, No. 3 (2013), 283–291
Suggested Citation
Ornuma Singha, Kanchana Kengkoom, Khuanjit Chaimongkolnukul, Sompong Cherdyu, Emsri Pongponratn, Taweesak Ketjareon, Yaowaluk Panavechkijkul, Sumate Ampawong Pulmonary Edema Due to Oral Gavage in a Toxicological Study Related to Aquaporin-1, -4 and -5 Expression. Journal of Toxicologic Pathology. Vol.26, No. 3 (2013), 283–291. doi:10.1293/tox.26.283 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/22824
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Title
Pulmonary Edema Due to Oral Gavage in a Toxicological Study Related to Aquaporin-1, -4 and -5 Expression
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.