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Updated: May 24, 2026
Histological Quantification of Chronic Myocardial Infarct in Rats
Published on: December 11, 2016
Myocardial remodeling after large infarcts in rat converts post rest-potentiation in force decay
Danilo Sales Bocalini1, Leonardo dos Santos, Ednei Luiz Antonio
1Departamento de Medicina, Divisão de Cardiologia, Universidade Federal de São Paulo, Brazil. bocalini@fcr.epm.br
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(+)/Ca(2+) 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.
