• Esra Sağlam, Ahmet Ozer Sehirli, Emine Nur Ozdamar, Gazi Contuk, Sule Cetinel, Derya Ozsavcı, Selami Süleymanoğlu, and Göksel Sener.
• Maltepe University, School of Medicine, Department of Pharmacology and Clinical Pharmacology, İstanbul, Turkey. esra.k.saglam@gmail.com.
• Ulus Travma Acil Cer. 2014 May 1;20(3):151-60.

BackgroundThis study was designed to determine the possible protective effect of captopril treatment against oxidative damage in heart and lung tissues induced by burn injury.MethodsUnder 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-α (TNF-α) as a pro-inflammatory cytokine, malondialdehyde and glutathione levels and myeloperoxidase, caspase-3, and Na+,K+-ATPase activity in addition to the histological analysis.ResultsBurn injury caused significant alterations in left ventricular function. In heart and lung tissues, TNF-α 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.ConclusionCaptopril prevents burn-induced damage in heart and lung tissues and protects against oxidative organ damage.

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