Myocardial Remodeling after Large Infarcts in Rat Converts Post Rest-Potentiation in Force Decay


Autoria(s): Bocalini, Danilo Sales; dos-Santos, Leonardo; Antonio, Ednei Luiz; dos Santos, Alexandra Alberta; Davel, Ana Paula Couto; Rossoni, Luciana Venturini; Vassallo, Dalton Valentim; Tucci, Paulo José Ferreira
Contribuinte(s)

UNIVERSIDADE DE SÃO PAULO

Data(s)

01/11/2013

01/11/2013

2012

Resumo

Background: Post-rest contraction (PRC) of cardiac muscle provides indirect information about the intracellular calcium handling. Objective: Our aim was to study the behavior of PRC, and its underlying mechanisms, in rats with myocardial infarction. Methods: Six weeks after coronary occlusion, the contractility of papillary muscles (PM) obtained from sham-operated (C, n = 17), moderate infarcted (MMI, n = 10) and large infarcted (LMI, n = 14) rats was evaluated, following rest intervals of 10 to 60 seconds before and after incubation with lithium chloride (Li+) substituting sodium chloride or ryanodine (Ry). Protein expression of SR Ca(2+)-ATPase (SERCA2), Na+/Ca2+ exchanger (NCX), phospholamban (PLB) and phospho-Ser(16)-PLB were analyzed by Western blotting. Results: MMI exhibited reduced PRC potentiation when compared to C. Opposing the normal potentiation for C, post-rest decays of force were observed in LMI muscles. In addition, Ry blocked PRC decay or potentiation observed in LMI and C; Li+ inhibited NCX and converted PRC decay to potentiation in LMI. Although MMI and LMI presented decreased SERCA2 (72 +/- 7% and 47 +/- 9% of Control, respectively) and phospho-Ser(16)-PLB (75 +/- 5% and 46 +/- 11%, respectively) protein expression, overexpression of NCX (175 +/- 20%) was only observed in LMI muscles. Conclusion: Our results showed, for the first time ever, that myocardial remodeling after MI in rats may change the regular potentiation to post-rest decay by affecting myocyte Ca(2+) handling proteins. (Arq Bras Cardiol 2012;98(3):243-251)

Identificador

ARQUIVOS BRASILEIROS DE CARDIOLOGIA, RIO DE JANEIRO, v. 98, n. 3, supl. 1, Part 1-2, pp. 243-250, MAR, 2012

0066-782X

http://www.producao.usp.br/handle/BDPI/37547

10.1590/S0066-782X2012005000016

http://dx.doi.org/10.1590/S0066-782X2012005000016

Idioma(s)

eng

Publicador

ARQUIVOS BRASILEIROS CARDIOLOGIA

RIO DE JANEIRO

Relação

ARQUIVOS BRASILEIROS DE CARDIOLOGIA

Direitos

openAccess

Copyright ARQUIVOS BRASILEIROS CARDIOLOGIA

Palavras-Chave #VENTRICULAR REMODELING #MYOCARDIAL INFARCTION #MUSCLE RELAXATION #MUSCLE STRENGTH #RATS #HEART-FAILURE #FREQUENCY-RELATIONSHIP #VENTRICULAR MYOCYTES #RYANODINE RECEPTOR #FAILING HEARTS #CARDIAC-MUSCLE #CONTRACTILITY #PERFORMANCE #MECHANISMS #EXCHANGE #CARDIAC & CARDIOVASCULAR SYSTEMS
Tipo

article

original article

publishedVersion