Effect of NAD on recovery of adenine nucleotide pool, phosphorylation potential, and stimulation of apoptosis during late period of reperfusion damage to myocardium.

The system of energy supply in the myocardium of the left and right ventricles did not recover after short-term circulatory disturbances. ATP synthesis decreased in parallel with activation of poly-(ADP-ribose)-polymerase in the ischemic region of the right ventricle, extra-ischemic region, and in the left ventricle by 5.85, 5.4, and 2.2 times, respectively. Intravenous injection of NAD immediately after blood flow resumption in the subacute period of ischemia-reperfusion damage virtually completely normalized the pool of adenine nucleotides, energy change of the adenine nucleotide system, and phosphorylation potential. Exogenous NAD inhibited activity of poly-(ADP-ribose)-polymerase in the ischemic region of the right ventricle, extra-ischemic region, and in the ischemic region of the left ventricle by 2.4, 2.9, and 1.52 times, respectively. We hypothesize that NAD acts as a regulator of signal mechanism of apoptosis induction during ischemia-reperfusion damages to the myocardium.

[The subcellular pathophysiology of heart failure due to toxic-allergic myocarditis and the action of refracterin on intracardiac hemodynamics and the functional state of the 3 subcellular cardiomyocyte systems responsible for the act of contraction-relaxation]. / Subkletochnaia patofiziologiia nedostatochnosti serdtsa, obuslovennoi toksiko-allergicheskim miokarditom, i deistvie refrakterina na vnutriserdechnuiu gemodinamiku i funktsional'noe sostoianie trekh subkletochnykh sistem kardiomiotsita otvetstvennykh za akt sokrashchenie--rasslablenie.

It is shown that cardiotropic drug refracterin promotes recovery of cardiac contraction and relaxation, their coordination destroyed in cardiac failure (CF) caused by 10-day toxico-allergic myocarditis (TAM). Pumping capacity of the heart returns to normal after normalization of functional activity of three systems of cardiomyocyte responsible for contraction-relaxation: contractile proteins, energy supply and calcium transport. The key process is refracterin-related reestablishment of normal content and proportion of adenyl nucleotides and creatininephosphate and regulation role of phosphorylation and energy of metabolic processes in the cells and their interaction. Thus, refracterin effectiveness lies in its ability to interfere in intracellular metabolic processes in the myocardium, to reestablish normal homeostasis of the systems responsible for contraction-relaxation function and eventually to remove left ventricular cardiac dysfunction.