| Abstrakt: |
The relationship between purkinje fibre cells (PFC) and ventricular myocardium is the focus of this investigation. Ca2+ concentration mediates AP production under these conditions. Our theoretical framework is based on Aslandi's (2001) humanendocardial cell model (ALD). The ALD model is improved by the experimental data provided by Han on human PFC Ca2+ currents. While keeping the same threshold (0.05), G power (80%), confidence interval (95%) and enrollment ratio, we apply the Euler integration method to the same 100 data from the human PFC model and analyse it under various concentration failure scenarios (1:1). While the action potential (AP) is at -53.04 mV when exposed to 2 mM external Ca2+, it falls with increasing concentrations of Ca2+o in the prefrontal cortex (10%=2.2 mM, 25%=2.5 mM, 50%=3 mM, and 100%=4 mM). Ca2+o at 10% in the PFC is equivalent to 1.8 mM, 25% to 1.5 mM, 50% to 1 mM, and 100% to 0.1 mM, with corresponding AP values of -42.76, -53.89, -55.08, and -45.88 mV. AP for raising PFC Ca2+i by 10% (=1.1 mM), 25% (=1.25 mM), 50% (=1.5 mM), and 100% (=2 mM), and AP for lowering PFC Ca2+i by 10% (=-54.64 mV), 25% (=-50.38 mV), 50% (=-53.04 mV), and 100% (=-0.32 mV). When comparing healthy and diseased states, a wide range of values for the average L-type Ca2+ current (ICaL, measured in Pico Amperes [pA]) is seen. Normal and abnormal Ca2+ concentrations in intracellular and extracellular PFC modify the plateau phase, and longer-than-usual AP cycles are associated with heart failure. [ABSTRACT FROM AUTHOR] |
