Document Detail

Nandrolone decanoate determines cardiac remodelling and injury by an imbalance in cardiac inflammatory cytokines and ACE activity, blunting of the Bezold-Jarisch reflex, resulting in the development of hypertension.
MedLine Citation:
PMID:  23287648     Owner:  NLM     Status:  Publisher    
The aims of this study were to evaluate the effects of nandrolone (ND) on cardiac inflammatory cytokines, ACE activity, troponin I, and the sensitivity of the Bezold-Jarisch reflex (BJR). Male Wistar rats were administered either ND (20 mg/kg; DECA) or vehicle (control animals; CONT) for 4 weeks. BJR was analyzed by measuring the bradycardia and hypotension responses elicited by serotonin administration (2-32 μg/kg). Mean arterial pressure (MAP) was assessed and myocyte hypertrophy was determined by the heart weight/body weight ratio and by morphometric analysis. Matrix collagen deposition was assessed by histological analysis of the picrosirius red-stained samples. Mesenteric vascular reactivity was performed and central venous pressure (CVP) evaluated. Cardiac inflammatory cytokine levels and angiotensin-converting enzyme (ACE) activity were studied as well the biomarker of cardiac lesion, troponin I. DECA group showed enhancement of matrix type I collagen deposition (p<0.01) and cardiac ACE activity (p<0.01) compared with the CONT. Interleukin (IL)-10 was reduced (p<0.01) and pro-inflammatory cytokines (TNF-α and IL-6; p<0.01) were increased in the DECA group compared with CONT. Cardiac injury was observed in the DECA group shown by the reduction in cardiac troponin I (p<0.01) compared with the CONT group. Animals in the DECA group also developed myocyte hypertrophy and reduction of BJR sensitivity. The MAP of animals treated with ND reached hypertensive levels (p<0.01; compared with CONT). No changes in CVP and vascular reactivity were observed in both experimental groups. We conclude that high doses of ND elicit cardiotoxic effects with cardiac remodelling and injury. Cardiac changes reduce the BJR sensitivity. Together, these abnormalities contributed to the development of hypertension in animals in the DECA group.
João Vicente Maggioni Franquni; Andrews Marques do Nascimento; Eweliny Miranda de Lima; Girlândia Alexandre Brasil; Otávio Arruda Heringer; Karla Oliveira Dos Santos Cassaro; Thony Vinicius Pita da Cunha; Carlos Musso; Maria Carmen L F Silva Santos; Ieda Carneiro Kalil; Denise Coutinho Endringer; Giovanna Assis Pereirra Boëchat; Nazaré Souza Bissoli; Tadeu Uggere de Andrade
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-12-31
Journal Detail:
Title:  Steroids     Volume:  -     ISSN:  1878-5867     ISO Abbreviation:  Steroids     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2013-1-4     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0404536     Medline TA:  Steroids     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2012. Published by Elsevier Inc.
Department of Pharmacy, University of Vila Velha, Espírito Santo, Brazil.
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