Author/Authors :
Asgharian Rezaee, Mitra Department of Pharmacodynamics and Toxicology - School of Pharmacy - Mashhad University of Medical Sciences, Mashhad - Department of Toxicology and Pharmacology - Faculty of Pharmacy - Kerman University of Medical Sciences, Kerman - Pharmaceutical Research Center - Institute of Neuropharmacology - Kerman University of Medical Sciences , Moallem, Adel Department of Pharmacology and toxicology - Faculty of Pharmacy - University of Ahl Al Bayt, Karbala - Pharmaceutical Research Center - Mashhad University of Medical Sciences, Mashhad - Medical Toxicology Research Center, Mashhad University of Medical Sciences , Mohammadpour, Amir Hooshang Pharmaceutical Research Center - Mashhad University of Medical Sciences - Department of Pharmacodynamics and Toxicology - School of Pharmacy - Mashhad University of Medical Sciences , Mahmoudi, Mahmoud Immunology Research Center - School of Medicine - Mashhad University of Medical Sciences , Sankian, Mojtaba Immunobiochemistry Laboratory - Immunology Research Center - Bu-Ali Research Institute - School of Medicine - Mashhad University of Medical Sciences , Farzadnia, Mehdi Department of Pathology - School of Medicine - Imam Reza Hospital - Mashhad University of Medical Sciences , Alavi, Hassan Electron Microscope Unit - Bu-Ali Research Institute - Mashhad University of Medical Science - Mashhad - School of Medicine - Mashhad Branch - Islamic Azad University , Imenshahidi, Mohsen Pharmaceutical Research Center - Mashhad University of Medical Sciences - Department of Pharmacodynamics and Toxicology - School of Pharmacy - Mashhad University of Medical Sciences
Abstract :
Objective(s): Cardiotoxicity is one of the major consequences in carbon monoxide poisoning. Following our previous work, in this study we aimed to define the myocardium changes induced by carbon monoxide (CO) intoxication and evaluate erythropoietin (EPO) effect on CO cardiotoxicity in rat. Materials and Methods: Severe carbon monoxide toxicity induced by 3000 ppm CO in Wistar rat. EPO was administrated (5000 IU/Kg, intraperitoneal injection) at the end of CO exposure and then the animals were re-oxygenated with the ambient air. Subsequently heart was removed and assessed by histopathology and electron microscopy examinations.
Results: 3000 ppm CO induced significant myocardium injury; multiple foci of necrosis and lymphocyte infiltration compare with the control (P˂0.05). Electron microscopy examination showed myofibril lysis and mitochondrial swelling in myocardium due to 3000 ppm CO poisoning. However EPO administration after CO exposure resulted in significant reduction in cardiomyocytes injury (P˂0.05). Conclusion: Our results represented protective effect of EPO on cardiac injury induced by CO intoxication in rat.
Keywords :
Carbon monoxide poisoning , Cardiotoxicity , Erythropoietin , Histopathology , Rat
