Исследована активность каспазы 3 и каспазы 8 в ткани миокарда кроликов при острой гемодинамической перегрузке левого желудочка, вызванной стенозом восходящей аорты.
Intensification of cardiomyocyte apoptotic death is considered by many authors to be a very important element in the development of cardiac insufficiency. In this connection a detailed study of molecular mechanizms underlying this phenomenon under different types of cardio-vascular pathology is of great interest. It is well known that particularly chronic overload of the left ventricle is accompanied by induced cardiomyocyte apoptosis. Meanwhile the response of programmed cell death to an acute cardiac overload is still poorly investigated. The experiment was performed on adult male Chinchilla rabbits in which an acute left ventricular overload was modeled by the ascending aorta banding by 1/3 of its initial diameter. 1, 3 and 5 days later caspase 3 and caspase 8 activity was evaluated in the myocardium of the left and right ventricles (LV and RV). It was found that caspase 3 activity significantly increases in both ventricles of the heart indicating the induction of myocardial cell apoptosis. Caspase 8 activity significantly rises in the LV and does not change in the right ventricle (RV) which allows us to conclude that extrinsic mechanizms take part in apoptotic cell death in the LV, but in the RV apoptogenic signal is only transmitted through the intrinsic (mitochondrial) pathway.