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Tramadol Alleviates Myocardial Injury Induced by Acute Hindlimb Ischemia Reperfusion in Rats
BACKGROUND: Organ injury occurs not only during periods of ischemia but also during reperfusion. It is known that ischemia reperfusion (IR) causes both remote organ and local injuries. OBJECTIVE: This study evaluated the effects of tramadol on the heart as a remote organ after acute hindlimb IR. MET...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Sociedade Brasileira de Cardiologia
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4559124/ https://www.ncbi.nlm.nih.gov/pubmed/26039663 http://dx.doi.org/10.5935/abc.20150059 |
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author | Takhtfooladi, Hamed Ashrafzadeh Asl, Adel Haghighi Khiabanian Shahzamani, Mehran Takhtfooladi, Mohammad Ashrafzadeh Allahverdi, Amin Khansari, Mohammadreza |
author_facet | Takhtfooladi, Hamed Ashrafzadeh Asl, Adel Haghighi Khiabanian Shahzamani, Mehran Takhtfooladi, Mohammad Ashrafzadeh Allahverdi, Amin Khansari, Mohammadreza |
author_sort | Takhtfooladi, Hamed Ashrafzadeh |
collection | PubMed |
description | BACKGROUND: Organ injury occurs not only during periods of ischemia but also during reperfusion. It is known that ischemia reperfusion (IR) causes both remote organ and local injuries. OBJECTIVE: This study evaluated the effects of tramadol on the heart as a remote organ after acute hindlimb IR. METHODS: Thirty healthy mature male Wistar rats were allocated randomly into three groups: Group I (sham), Group II (IR), and Group III (IR + tramadol). Ischemia was induced in anesthetized rats by left femoral artery clamping for 3 h, followed by 3 h of reperfusion. Tramadol (20 mg/kg, intravenous) was administered immediately prior to reperfusion. At the end of the reperfusion, animals were euthanized, and hearts were harvested for histological and biochemical examination. RESULTS: The levels of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were higher in Groups I and III than those in Group II (p < 0.05). In comparison with other groups, tissue malondialdehyde (MDA) levels in Group II were significantly increased (p < 0.05), and this increase was prevented by tramadol. Histopathological changes, including microscopic bleeding, edema, neutrophil infiltration, and necrosis, were scored. The total injuryscore in Group III was significantly decreased (p < 0.05) compared with Group II. CONCLUSION: From the histological and biochemical perspectives, treatment with tramadol alleviated the myocardial injuries induced by skeletal muscle IR in this experimental model. |
format | Online Article Text |
id | pubmed-4559124 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Sociedade Brasileira de Cardiologia |
record_format | MEDLINE/PubMed |
spelling | pubmed-45591242015-09-04 Tramadol Alleviates Myocardial Injury Induced by Acute Hindlimb Ischemia Reperfusion in Rats Takhtfooladi, Hamed Ashrafzadeh Asl, Adel Haghighi Khiabanian Shahzamani, Mehran Takhtfooladi, Mohammad Ashrafzadeh Allahverdi, Amin Khansari, Mohammadreza Arq Bras Cardiol Original Article BACKGROUND: Organ injury occurs not only during periods of ischemia but also during reperfusion. It is known that ischemia reperfusion (IR) causes both remote organ and local injuries. OBJECTIVE: This study evaluated the effects of tramadol on the heart as a remote organ after acute hindlimb IR. METHODS: Thirty healthy mature male Wistar rats were allocated randomly into three groups: Group I (sham), Group II (IR), and Group III (IR + tramadol). Ischemia was induced in anesthetized rats by left femoral artery clamping for 3 h, followed by 3 h of reperfusion. Tramadol (20 mg/kg, intravenous) was administered immediately prior to reperfusion. At the end of the reperfusion, animals were euthanized, and hearts were harvested for histological and biochemical examination. RESULTS: The levels of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were higher in Groups I and III than those in Group II (p < 0.05). In comparison with other groups, tissue malondialdehyde (MDA) levels in Group II were significantly increased (p < 0.05), and this increase was prevented by tramadol. Histopathological changes, including microscopic bleeding, edema, neutrophil infiltration, and necrosis, were scored. The total injuryscore in Group III was significantly decreased (p < 0.05) compared with Group II. CONCLUSION: From the histological and biochemical perspectives, treatment with tramadol alleviated the myocardial injuries induced by skeletal muscle IR in this experimental model. Sociedade Brasileira de Cardiologia 2015-08 /pmc/articles/PMC4559124/ /pubmed/26039663 http://dx.doi.org/10.5935/abc.20150059 Text en http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Takhtfooladi, Hamed Ashrafzadeh Asl, Adel Haghighi Khiabanian Shahzamani, Mehran Takhtfooladi, Mohammad Ashrafzadeh Allahverdi, Amin Khansari, Mohammadreza Tramadol Alleviates Myocardial Injury Induced by Acute Hindlimb Ischemia Reperfusion in Rats |
title | Tramadol Alleviates Myocardial Injury Induced by Acute Hindlimb Ischemia
Reperfusion in Rats |
title_full | Tramadol Alleviates Myocardial Injury Induced by Acute Hindlimb Ischemia
Reperfusion in Rats |
title_fullStr | Tramadol Alleviates Myocardial Injury Induced by Acute Hindlimb Ischemia
Reperfusion in Rats |
title_full_unstemmed | Tramadol Alleviates Myocardial Injury Induced by Acute Hindlimb Ischemia
Reperfusion in Rats |
title_short | Tramadol Alleviates Myocardial Injury Induced by Acute Hindlimb Ischemia
Reperfusion in Rats |
title_sort | tramadol alleviates myocardial injury induced by acute hindlimb ischemia
reperfusion in rats |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4559124/ https://www.ncbi.nlm.nih.gov/pubmed/26039663 http://dx.doi.org/10.5935/abc.20150059 |
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