PDF(Pubmed)
Abstract：
Dysfunctional Ca2+ signaling affects the myocardial systole and diastole, may trigger arrhythmia and cause transcriptomic and proteomic modifications in heart failure. Thus, synchronous real-time measurement of Ca2+ and force is essential to investigate the relationship between contractility and Ca2+ signaling and the alteration of excitation-contraction coupling (ECC) in human failing myocardium. Here, we present a method for synchronized acquisition of intracellular Ca2+ and contraction force in long-term cultivated slices of human failing myocardium. Synchronous time series of contraction force and intracellular Ca2+ were used to calculate force-calcium loops and to analyze the dynamic alterations of ECC in response to various pacing frequencies, post-pause potentiation, high mechanical preload and pharmacological interventions in human failing myocardium. We provide an approach to simultaneously and repeatedly investigate alterations of contractility and Ca2+ signals in long-term cultured myocardium, which will allow detecting the effects of electrophysiological or pharmacological interventions on human myocardial ECC.
摘要：
功能失调的Ca2+信号影响心肌收缩和舒张，可能引发心律失常并引起心力衰竭的转录组和蛋白质组修饰。因此，同步实时测量Ca2和力对于研究人衰竭心肌中收缩性和Ca2信号传导与兴奋-收缩耦合（ECC）的变化之间的关系至关重要。这里,我们提出了一种在长期培养的人衰竭心肌切片中同步获取细胞内Ca2和收缩力的方法。使用收缩力和细胞内Ca2的同步时间序列来计算力-钙回路，并分析ECC响应于各种起搏频率的动态变化，暂停后增强，人类衰竭心肌的高机械预紧力和药物干预。我们提供了一种方法，可以同时重复地研究长期培养的心肌中收缩性和Ca2信号的变化，这将允许检测电生理或药物干预对人心肌ECC的影响。
