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Histopathological study of erythropoietin protective effect on carbon monoxide-induced cardiotoxicity in rat
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. MATERIAL...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Mashhad University of Medical Sciences
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5749351/ https://www.ncbi.nlm.nih.gov/pubmed/29299194 http://dx.doi.org/10.22038/IJBMS.2017.9471 |
Sumario: | 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. |
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