Block of Electrical Excitation Conduction During the Development of Ischemia in a Mathematical Model of Cardiac Tissue

In this work, we studied the effects of acute ischemia in a human cardiomyocyte model and in a one-dimensional tissue model. In the human cardiomyocyte model, changes in <tex xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">[ATP]ᵢ</tex> and <tex xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">[K⁺]ₒ</tex> caused an increase in the activity of the ATP-dependent K+ membrane current IKATP, resulting in an increase in the resting potential and a decrease in the duration of the action potential in cardiomyocytes after 5,10, and 15 minutes of simulated acute ischemia. A decrease in the contractile force of cardiomyocytes was observed in the 15th minute of simulated ischemia. Simulating 15 minutes of acute ischemia in a 1D model of myocardial tissue, we obtained a block for conduction of electrical excitation along a virtual fiber. The reason for the block is a decrease in the amplitude of the fast sodium current due to the rise of the resting potential during ischemia. In addition, the electromechanical interaction of the cardiomyocytes in the tissue decreases the potential-dependent conductance of the gate of the sodium channels more and more from stimulus to stimulus. A compensatory mechanism was found to restore the conduction of excitation along the 1D tissue. This mechanism was shown to slow the velocity of excitation propagation along the fiber during ischemia, which is associated with weakening of the conductance of the intercellular gap junctions.