The article is devoted to the study of the myocardium structural reorganization features under the action of 0,01 LD50 of mercury chloride (II) rats when comparing chronic (30 injections) and subchronic (10 injections) exposures. Structural-metabolic reorganization of the myocardium was studied using histological, histochemical and electron microscopic methods. Computer morphometric analysis with subsequent statistical processing was applied. It was established that the main mechanisms of cardiotoxic effect of mercuric chloride are: hypoxia (due to damage to micro vessels; disorder of myogenic regulation at the expense of damage intercalated discs) and the appearance of cell detrits and abnormal proteins as a result of the destruction of cardiomyocytes. Sensitive to the toxic effects of chloride mercuric in low doses are myofibrils, sarcoplasmic network and the energy apparatus of cardiomyocytes - the mitochondria. It was found that chronic exposure to low doses of mercuric chloride causes non-specific qualitative and quantitative changes in all structural components of the heart, damage to the tissue barrier is ongoing and dynamic and resorptive insufficiency hemomicrocirculatory bed of the heart that leads to chronic swelling that causes the development of diffuse fibrosis and enhances cardiac decompensation activities.