Cellular energetic extension applied to the Luo-Rudy II ventricular cell model

The goal of this study is to introduce a new ventricular cell energetic model extension that, in contrast to earlier presented dynamic cell models, allows the simulation of long-term pathological events such as development of hypoxia and anoxia. We created an energetic ventricular cell model extension that involves the adenosine triphosphate (ATP)-adenosine diphosphate (ADP) cycling mechanism. We chose the well known Luo-Rudy II (LR) ventricular model and extended it with the developed energetic circulation system, so that we can easily validate the obtained results. The presence of hypoxia reduces the ATP concentration. In LR model a 10%/25%/50%/75% ATP concentration decrease subdued the ionic pumps efficiency by: 4%/14%/32%/55% for calcium pump of the sarcoplasmic reticulum; 3%/11%/26%/45% for external membranous calcium pump; 3%/10%/22%/39% for calcium sodium exchanger; and 2%/8%/18%/33% for sodium potassium exchanger. The malfunction of the calcium regulation mechanism is the principal danger factor in presence of hypoxia or anoxia and it is the most sensible element during ischemia.