Captopril protects against burn-induced cardiopulmonary injury in rats
Autor: | Şule Çetinel, Göksel Şener, Emine Nur Ozdamar, Esra Sağlam, Derya Özsavcı, Gazi Contuk, Ahmet Ozer Sehirli, Selami Süleymanoğlu |
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Přispěvatelé: | Saglam, Esra, Sehirli, Ahmet Ozer, Ozdamar, Emine Nur, Contuk, Gazi, Cetinel, Sule, Ozsavci, Derya, Suleymanoglu, Selami, Sener, Goksel, Maltepe Üniversitesi |
Rok vydání: | 2014 |
Předmět: |
Male
Burn injury Captopril CONVERTING-ENZYME-INHIBITORS medicine.medical_treatment CARDIOMYOCYTES Electrocardiography chemistry.chemical_compound cytokine FAILURE Lung TUMOR-NECROSIS-FACTOR biology Caspase 3 lipid peroxidation Heart Malondialdehyde Glutathione myeloperoxidase RENIN-ANGIOTENSIN SYSTEM medicine.anatomical_structure Cytokine Anesthesia Myeloperoxidase Emergency Medicine MYOCARDIAL DAMAGE Female Tumor necrosis factor alpha Sodium-Potassium-Exchanging ATPase Burns medicine.drug Thoracic Injuries Protective Agents medicine Animals Rats Wistar REMOTE ORGANS thermal trauma Tumor Necrosis Factor-alpha business.industry Myocardium CIRCULATING LEVELS Rats Anesthesiology and Pain Medicine chemistry biology.protein Surgery business INDUCED OXIDATIVE INJURY |
Zdroj: | Turkish Journal of Trauma and Emergency Surgery. 20:151-160 |
ISSN: | 1307-7945 1306-696X |
Popis: | WOS: 000337163600001 PubMed ID: 24936835 BACKGROUND: This study was designed to determine the possible protective effect of captopril treatment against oxidative damage in heart and lung tissues induced by burn injury. METHODS: Under ether anesthesia, the shaved dorsum of Wistar albino rats was exposed to 90 C water bath for 10 seconds. Captopril was administered intraperitoneally (10 mg/kg) after the burn injury and repeated twice daily. In the sham group, the dorsum was dipped in a 25 C water bath for 10 seconds. At the end of the 24 hours, echocardiographic recordings were performed, then animals were decapitated and heart and lung tissue samples were taken for the determination of tumor necrosis factor-alpha (TNF-alpha) as a pro-inflammatory cytokine, malondialdehyde and glutathione levels and myeloperoxidase, caspase-3, and Na+, K+-ATPase activity in addition to the histological analysis. RESULTS: Burn injury caused significant alterations in left ventricular function. In heart and lung tissues, TNF-a and malondialdehyde levels and myeloperoxidase and caspase-3 activities were found to be increased, while glutathione levels and Na+, K+-ATPase activity were decreased due to burn injury. Captopril treatment significantly elevated the reduced glutathione level and Na+, K+-ATPase activity, and decreased cytokine and malondialdehyde levels and myeloperoxidase and caspase-3 activities. CONCLUSION: Captopril prevents burn-induced damage in heart and lung tissues and protects against oxidative organ damage. |
Databáze: | OpenAIRE |
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