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Right ventricular function following left myocardial infarction in rats with and without heart failure (864.6)
Author(s) -
Fernandes Aurélia,
Moura Viviane,
Siman Fabiana,
Ribeiro Júnior Rogério,
Dias Fernanda,
Jorge Zoghaib,
Vassallo Paula,
Vassallo Dalton,
Stefa Ivanita
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.864.6
Subject(s) - ventricle , inotrope , medicine , cardiology , contractility , heart failure , myocardial infarction , cardiac function curve , infarction , contraction (grammar)
It has been proposed that right ventricular function is an independent predictor of mortality and development of heart failure in patients with known left ventricle dysfunction following myocardial infarction (MI). This study was conducted to assess right ventricle (RV) contractility 8 weeks following MI in rats presenting a moderate to large infarct area. Myocardial infarction was induced in male Wistar rats to create transmural infarctions involving 40‐60% of the left ventricle surface. Infarct rats were divided in two groups: those that presented classical signs of heart failure (HF group) and those that did not (INF group), and these two groups were used to study isometric contraction in isolated RV strips. Inotropic responses in the RV strips were preserved in the INF group but were reduced in the HF group (3.75 mM Ca2+ treatment: Sham=163±18; INF=148±19; HF=68±11 g/mg*; *p<0.05); (5x10‐5 M Isoproterenol treatment: Sham=151±15, INF=134±17, HF=52±7 g/mg*; *p<0.05). The infarcted group without signs of HF showed preserved contractility in RV strips in response to post‐rest potentiation, increases in extracellular Ca2+ and isoproterenol treatment. Indeed, SERCA‐2a protein expression was increased in the INF group but not in the HF group. In conclusion, increased SERCA‐2a protein expression may play a role in the preservation of RV function post‐MI. Therefore, therapeutic strategies that attempt to increase SERCA‐2a protein expression levels may be useful for the treatment of HF. Grant Funding Source : Supported by FAPES and CNPq