Remodelamento miocárdico após grandes infartos converte potencia？？o pós-pausa em decaimento da for？a em ratos

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-ser16-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.