Апоптоз кардиомиоцитов при вазоренальной артериальной гипертензии как следствие нарушения энергетического баланса клеток

Aim. To investigate the effects of phosphocreatine and ethylmethylhydroxypyridine succinate on cardiomyocyte apoptosis intensity and degree of ventricular cardiomyocytes hypertrophy in rabbits with vasorenal hypertension (VH) model. Methods. VH was modeled on rabbits by artificial abdominal aortic stenosis by one-third of the diameter just above the renal arteries arising. Rabbits were divided to 4 groups: rabbits with 4-week VH without treatment, rabbits with 4-week VH treated with phospho-creatine, rabbits with 4-week VH treated with ethylmethylhydroxypyridine succinate, and healthy rabbits (control group). Cardiomyocyte apoptosis intensity and degree of ventricular cardiomyocytes hypertrophy was assessed in all of the rabbits by evaluation of nuclear-cytoplasmic ratio. Results. Use of phosphocreatine or ethylmethylhydroxypyridine succinate led to a significant reduction of the apoptotic index in the left ventricular myocardium, whereas the similar effect on the right ventricle was only typical for phosphocreatine. None of these drugs had an effect on myocardial hypertrophy degree, which remained on the same level as in the untreated hypertensive animals. Conclusions. Energy deficiency is one of the factors inducing cardiomyocyte apoptosis, so administration of phosphocreatine or ethylmethylhydroxypyridine succinate might be an important component of heart failure prevention and treatment in hypertension. Myocardial hypertrophy has no effect on the cardiomyocyte apoptosis intensity in case of proper energy supply.