Ventricular fibrillation induced by 2-aminoethoxydiphenyl borate under conditions of hypoxia/reoxygenation.

Background: Ventricular fibrillation is an electrophysiological disorder leading to cardiac arrest that can be caused using chemicals. The 2-aminoethoxydiphenyl borate (2-apb) is a poorly understood compound that modulates store operated calcium entry and gap junctions and can provoke ventricular fibrillation. Our study aimed to investigate the effect of 2-apb on the work of an isolated rat heart and coronary vessels under normoxic conditions, as well as under conditions of hypoxia/reoxygenation, that affect intracellular calcium.

Methods: In order to accomplish this task, we used Langendorff rat heart preparation and multi-electrode registration of bioelectric activity of the heart with flexible arrays. An analysis of changes in the volume of coronary blood flow was also performed.

Results: Arrhythmogenic effect of 2-apb on an isolated rat heart was shown: an increase in the frequency and variability of the heart rhythm, a decrease in the electrical conductivity of the myocardium, and the appearance of ventricular fibrillation. Under hypoxic conditions, the arrhythmogenic effect of 2-apb decreased and no ventricular fibrillation was observed. In addition, 2-apb had a stabilizing effect on coronary vessels and weakened the effect of reoxygenation on the electrical activity of the heart.

Conclusions: Obtained results indicate that the effect of arrhythmogenic chemicals, for example, proarrhythmic drugs that affect the myocardial [Ca²⁺]in, depended on the oxygen supply to the heart. The components of the store operated calcium entry and gap junctions can become promising therapeutic targets for controlling the physiological disorders of the heart and blood vessels caused or accompanied by reoxygenation.