Possible involvement of eicosanoids in alpha-naphthylthiourea-induced pulmonary oedema and alteration of angiotensin-converting enzyme activity
Autor: | Ercan Zs, Türker Rk, Eren S, Hakan Zengil |
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Rok vydání: | 1993 |
Předmět: |
Male
medicine.medical_specialty Pleural effusion alpha-Naphthylthiourea Pulmonary Edema In Vitro Techniques Peptidyl-Dipeptidase A chemistry.chemical_compound Internal medicine Edema Medicine Animals Lung Pharmacology chemistry.chemical_classification biology business.industry Respiratory disease Thiourea Angiotensin-converting enzyme Rats Inbred Strains General Medicine respiratory system medicine.disease respiratory tract diseases Rats Perfusion Enzyme Endocrinology medicine.anatomical_structure chemistry Lung oedema biology.protein Eicosanoids Female medicine.symptom business |
Zdroj: | Pharmacology. 46(5) |
ISSN: | 0031-7012 |
Popis: | alpha-Naphthylthiourea (ANTU) when injected intraperitoneally to rats at a dose of 10 mg/kg elicited lung oedema indicated by an increase in lung weight/body weight (LW/BW) ratio and pleural effusion. The injection of acetylsalicylic acid, which is a cyclo-oxygenase inhibitor, and BW 755C, a cyclo-oxygenase and lipoxygenase inhibitor, prior to ANTU produced a significant inhibition in pleural fluid accumulation without changing the LW/BW ratio. BW A4C, a selective 5-lipoxygenase inhibitor, however, caused a highly significant inhibition in pleural effusion and a slight but significant decrease in LW/BW ratio. Thromboxane A2 synthetase inhibitor, UK 38485, caused a slight but significant inhibition in pleural fluid accumulation without altering the LW/BW ratio. Iloprost, however, produced a slight but significant inhibition in the LW/BW ratio without reducing the pleural effusion rate. A significant decrease in angiotensin-converting enzyme (ACE) activity in the isolated perfused lungs of ANTU-treated rats was noted. This observation was thought to be an evidence of a functional alteration of the lung vascular endothelium. The possible role of eicosanoids in lung oedema induced by ANTU and the related mechanisms of decreased ACE activity are discussed. |
Databáze: | OpenAIRE |
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