Courtemanche M, Ramirez R J, Nattel S
Research Center, Montreal Heart Institute, Montreal, Quebec H1T 1C8, Canada.
Am J Physiol. 1998 Jul;275(1):H301-21. doi: 10.1152/ajpheart.1998.275.1.H301.
The mechanisms underlying many important properties of the human atrial action potential (AP) are poorly understood. Using specific formulations of the K+, Na+, and Ca2+ currents based on data recorded from human atrial myocytes, along with representations of pump, exchange, and background currents, we developed a mathematical model of the AP. The model AP resembles APs recorded from human atrial samples and responds to rate changes, L-type Ca2+ current blockade, Na+/Ca2+ exchanger inhibition, and variations in transient outward current amplitude in a fashion similar to experimental recordings. Rate-dependent adaptation of AP duration, an important determinant of susceptibility to atrial fibrillation, was attributable to incomplete L-type Ca2+ current recovery from inactivation and incomplete delayed rectifier current deactivation at rapid rates. Experimental observations of variable AP morphology could be accounted for by changes in transient outward current density, as suggested experimentally. We conclude that this mathematical model of the human atrial AP reproduces a variety of observed AP behaviors and provides insights into the mechanisms of clinically important AP properties.
人们对人类心房动作电位（AP）许多重要特性背后的机制了解甚少。基于从人类心房肌细胞记录的数据，利用钾离子、钠离子和钙离子电流的特定公式，以及泵电流、离子交换电流和背景电流的表示形式，我们建立了一个动作电位的数学模型。该模型动作电位类似于从人类心房样本记录的动作电位，并以类似于实验记录的方式对心率变化、L型钙电流阻断、钠/钙交换体抑制以及瞬时外向电流幅度变化作出反应。动作电位时程的心率依赖性适应是心房颤动易感性的一个重要决定因素，这归因于快速心率下L型钙电流从失活状态的不完全恢复以及延迟整流电流的不完全失活。如实验所表明的，动作电位形态变化的实验观察结果可以通过瞬时外向电流密度的变化来解释。我们得出结论，这个人类心房动作电位的数学模型再现了各种观察到的动作电位行为，并为临床上重要的动作电位特性的机制提供了见解。
