Triphosphoric Acid, Donated, Restores Heart Rhythm Disturbances Caused by Energetically Deficient, Mitochondrial Hypercalcaemia to Ca++ Mpt Pore Lesion

Ca ++ mPT pore damage leads to Ca ++ in the mitochondria (M), where Ca ++ pumps H + and pH, through the disordered depolarization electric potential of the internal M membrane, ATP synthesis is also afect, which is manifested by a mitochondrial energy deficit (MED). MED provoke cell hypo -anergyoxidative stress, OS collapse MM swells osmotic demyelinationmembrane rupture Mdetritus mass output with large molecule in intermembrane space Min cell cytosolapoptosis-inducing factorcytochrome Cwhich are the predictors of programmed cell death. Contributing to the increase in blood pressure to OS not only hyperadrenalinemia, but also the reduction of the effect of vasorelaxation by NO, which as it becomes becomes a trap for the excess oxygen free radicals, especially for oxygen superoxide. Triphosphoric acid (ATP), donated, as an energetic carrier, mitochondrial permeability transition pore-dependent Ca++uniporter, mPT pore, restores the disorder of electrical cardiac potentials: Conductivity, refractoriness of the atrioventricular node, sinus nodule automatism, and primary hypertension, caused by MED and, further, manifested by the microcirculatory and mitochondrial distress syndrome. Simultaneously, ATP influences: Mitochondrial ATP-dependent potassium channel, mitoKATP; acetylcholinedependent potassium channel, KACh cholinergic-M receptor; receptors: Adenosine A1; and purine P2. M myocardial cells create mesh nets that limit the disordered energy flow in the reduced M space, avoiding damage to the entire heart muscle. As a result, M also plays the role of the electroconductivity switch, which protects the heart from the extent of the damage of a "short circuit" in area necrotizing myocardiocytes and M hypoanergic. Hence, the anti-arrhythmogenic effect of ATP-energetic