title: Captopril protects against burn-induced cardiopulmonary injury in rats.
abstract: 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-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.
  
  
  RESULTS
  Burn 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.
  
  
  CONCLUSIONS
  Captopril prevents burn-induced damage in heart and lung tissues and protects against oxidative organ damage.
authors.affiliation: Maltepe University, School of Medicine, Department of Pharmacology and Clinical Pharmacology, İstanbul, Turkey. esra.k.saglam@gmail.com.
authors.forename: Esra
authors.initials: E
authors.lastname: Sağlam
authors.affiliation: Department of Pharmacology, Marmara University Faculty of Pharmacy, İstanbul, Turkey.
authors.forename: Ahmet Ozer
authors.initials: AO
authors.lastname: Sehirli
authors.affiliation: Department of Medical Pharmacology, Marmara University Faculty of Medicine, İstanbul, Turkey.
authors.forename: Emine Nur
authors.initials: EN
authors.lastname: Ozdamar
authors.affiliation: Department of Histology & Embryology, Marmara University Faculty of Medicine, İstanbul, Turkey.
authors.forename: Gazi
authors.initials: G
authors.lastname: Contuk
authors.affiliation: Department of Histology & Embryology, Marmara University Faculty of Medicine, İstanbul, Turkey.
authors.forename: Sule
authors.initials: S
authors.lastname: Cetinel
authors.affiliation: Department of Biochemistry, Marmara University Faculty of Pharmacy, İstanbul, Turkey.
authors.forename: Derya
authors.initials: D
authors.lastname: Ozsavcı
authors.affiliation: Department of Cardiology, Gulhane Military Medical Academy, İstanbul, Turkey.
authors.forename: Selami
authors.initials: S
authors.lastname: Süleymanoğlu
authors.affiliation: Department of Pharmacology, Marmara University Faculty of Pharmacy, İstanbul, Turkey.
authors.forename: Göksel
authors.initials: G
authors.lastname: Sener
mesh_terms: D000818:Animals; D002056:Burns / Q000378:metabolism*; D002216:Captopril / Q000494:pharmacology*; D053148:Caspase 3 / Q000378:metabolism; D004562:Electrocardiography; D005260:Female; D005978:Glutathione / Q000378:metabolism; D006321:Heart / Q000187:drug effects*; D008168:Lung / Q000737:chemistry / Q000187:drug effects* / Q000473:pathology; D008297:Male; D009206:Myocardium / Q000737:chemistry / Q000473:pathology; D020011:Protective Agents / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013898:Thoracic Injuries / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D020011:Protective Agents; D014409:Tumor Necrosis Factor-alpha; D002216:Captopril; D053148:Caspase 3; D000254:Sodium-Potassium-Exchanging ATPase; D005978:Glutathione