Schouten V J, van Deen J K, de Tombe P, Verveen A A
Biophys J. 1987 Jan;51(1):13-26. doi: 10.1016/S0006-3495(87)83307-6.
A mathematical model was derived that describes peak force of contraction as a function of stimulus interval and stimulus number in terms of Ca2+ transport between three hypothetical Ca2+ compartments. It includes the conventional uptake and release compartments and recirculation of a fraction r of the activator Ca2+. Peak force is assumed to be proportional to the amount of activator Ca2+ released from the release compartment into the sarcoplasm. A new extension is a slow exchange of Ca2+ with the extracellular space via an exchange compartment. Six independent parameters were necessary to reproduce the different effects of postextrasystolic potentiation, frequency potentiation, and post-rest potentiation in isolated heart muscle from the rat. The normalized steady state peak force (F/Fmax) under standard conditions varied by a factor of ten between preparations from rat heart. Analysis with the model indicated that most of this variation was caused by two variables: the Ca2+ influx per excitation and the recirculating fraction of activator Ca2+. The influence of the Ca2+ antagonist nifedipine of the force-interval relationship was reproduced by the model. It is concluded that the model may serve to analyze the variability of contractile force and the mode of actions of drugs in heart muscle.
推导了一个数学模型，该模型根据三个假设的钙离子区室之间的钙离子转运，将收缩峰值力描述为刺激间隔和刺激次数的函数。它包括传统的摄取和释放区室以及一部分（r）激活钙离子的再循环。假定峰值力与从释放区室释放到肌浆中的激活钙离子量成正比。一个新的扩展是通过一个交换区室使钙离子与细胞外空间进行缓慢交换。为了重现大鼠离体心肌中早搏后增强、频率增强和静息后增强的不同效应，需要六个独立参数。在标准条件下，大鼠心脏不同标本的归一化稳态峰值力（F/Fmax）相差十倍。该模型分析表明，这种变化大部分是由两个变量引起的：每次兴奋时的钙离子内流和激活钙离子的再循环分数。该模型重现了钙离子拮抗剂硝苯地平对力-间隔关系的影响。得出的结论是，该模型可用于分析心肌收缩力的变异性以及药物的作用方式。
