Biochemical assessment of simulation of deep noncoronarogenic myocardial damage

Considering the important role in the development of cardiomyocyte damage during ischemia, post-ischemic reperfusion, post-hypoxic reoxygenation and the so-called calcium paradox of the Na+-Ca2+ exchange system and Na+-H+ exchange, a model for the formation of non-coronarogenic myocardial necrosis by activating the Na+-Ca2+ exchange process has been proposed due to varying the composition of solutions, leading to changes in intracellular pH. The formation of cardiomyocyte damage was achieved by perfusion of the heart with a hyposodium solution. It was revealed that perfusion of the heart with a hyposodium environment with the replacement of sodium chloride by ammonium chloride is accompanied by an intense release of myoglobin from the heart and the appearance of significant amounts of adenosine in the perfusion solution flowing from the heart with a simultaneous increase in diastolic pressure. In turn, the use of potassium chloride does not lead to the release of adenosine or myoglobin into the outflowing perfusion solution and is accompanied by a short-term, slight increase in diastolic pressure. Thus, only when ammonium chloride was used to replace sodium chloride, deep and irreversible damage to cardiomyocytes was observed.