Departamento de Medicina, Divisão de Cardiologia, Universidade Federal de São Paulo, Brazil.
Arq Bras Cardiol. 2012 Mar;98(3):243-51. doi: 10.1590/s0066-782x2012005000016. Epub 2012 Feb 16.
Post-rest contraction (PRC) of cardiac muscle provides indirect information about the intracellular calcium handling.
Our aim was to study the behavior of PRC, and its underlying mechanisms, in rats with myocardial infarction.
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.
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.
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.
心肌的后收缩（PRC）提供了细胞内钙处理的间接信息。
我们的目的是研究心肌梗死后大鼠 PRC 的行为及其潜在机制。
在冠状动脉闭塞 6 周后，评估来自假手术（C，n=17）、中度梗死（MMI，n=10）和大面积梗死（LMI，n=14）大鼠的乳头肌（PM）的收缩性，在孵育氯化锂（Li(+））替代氯化钠或兰尼碱（Ry）前后，休息间隔为 10 至 60 秒。通过 Western blot 分析肌浆网 Ca(2+)-ATP 酶（SERCA2）、Na(+)/Ca(2+)交换体（NCX）、磷酸化肌球蛋白结合蛋白（PLB）和磷酸化 Ser(16)-PLB 的蛋白表达。
与 C 相比，MMI 表现出 PRC 增强作用减弱。与 C 的正常增强相反，在 LMI 肌肉中观察到后休息力衰减。此外，Ry 阻断了 LMI 和 C 中观察到的 PRC 衰减或增强；Li(+)抑制 NCX 并将 PRC 衰减转化为 LMI 中的增强。尽管 MMI 和 LMI 表现出 SERCA2 减少（分别为对照的 72±7%和 47±9%）和磷酸化 Ser(16)-PLB 减少（分别为 75±5%和 46±11%），但仅在 LMI 肌肉中观察到 NCX 的过度表达（175±20%）。
我们的研究结果首次表明，大鼠心肌梗死后的心肌重构可能通过影响心肌细胞 Ca(2+)处理蛋白而将正常增强转变为后休息力衰减。
