Key Laboratory of Biomedical Information Engineering of Education Ministry, Institute of Biomedical Analytical Technology and Instrumentation, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China; School of Biomedical Engineering, Capital Medical University, Beijing 100069, China.
Key Laboratory of Biomedical Information Engineering of Education Ministry, Institute of Biomedical Analytical Technology and Instrumentation, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710049, China.
Comput Methods Programs Biomed. 2014 Feb;113(2):690-6. doi: 10.1016/j.cmpb.2013.11.007. Epub 2013 Nov 20.
The ionic mechanism of change in short-term memory (STM) during acute myocardial ischemia has not been well understood. In this paper, an advanced guinea pig ventricular model developed by Luo and Rudy was used to investigate STM property of ischemic ventricular myocardium. STM response was calculated by testing the time to reach steady-state action potential duration (APD) after an abrupt shortening of basic cycling length (BCL) in the pacing protocol. Electrical restitution curves (RCs), which can simultaneously visualize multiple aspects of APD restitution and STM, were obtained from dynamic and local S1S2 restitution portrait (RP), which consist of a longer interval stimulus (S1) and a shorter interval stimulus (S2). The angle between dynamic RC and local S1S2 RC reflects the amount of STM. Our results indicated that compared with control (normal) condition, time constant of STM response in the ischemic condition decreased significantly. Meanwhile the angle which reflects STM amount is less in ischemic model than that in control model. By tracking the effect of ischemia on intracellular ion concentration and membrane currents, we declared that changes in membrane currents caused by ischemia exert subtle influences on STM; it is only the decline of intracellular calcium concentration that give rise to the most decrement of STM.
急性心肌缺血时短期记忆（STM）变化的离子机制尚未得到很好的理解。本文采用 Luo 和 Rudy 开发的先进豚鼠心室模型，研究缺血性心室心肌的 STM 特性。STM 响应通过测试起搏方案中基本循环长度（BCL）突然缩短后达到稳定动作电位持续时间（APD）的时间来计算。电恢复曲线（RC）可通过动态和局部 S1S2 恢复图（RP）同时可视化 APD 恢复和 STM 的多个方面，RP 由较长的间隔刺激（S1）和较短的间隔刺激（S2）组成。动态 RC 和局部 S1S2 RC 之间的角度反映了 STM 的量。结果表明，与对照（正常）条件相比，缺血条件下 STM 响应的时间常数显著降低。同时，与对照模型相比，缺血模型中反映 STM 量的角度较小。通过跟踪缺血对细胞内离子浓度和膜电流的影响，我们宣布缺血引起的膜电流变化对 STM 产生微妙影响；只有细胞内钙浓度的下降才导致 STM 最大程度的减少。
