Lead in conditions of prolonged intake of experimental animals into the body leads to the development of severe arterial hypertension, which develops as a result of a significant increase in total peripheral vascular resistance caused by the development of changes in the α1-adrenoreactivity of the cardiovascular system and the reactivity of the renin-angiotensin system. At the same time there is a decrease in the pumping function of the heart, which is manifested by a decrease in both the stroke and cardiac volume indices. The use of melaxen in conditions of prolonged lead poisoning has a significant therapeutic effect, which is characterized by a decrease in the severity of arterial hypertension, restoration of pumping function of the heart, and a decrease in the specific peripheral vascular resistance. The therapeutic use of melaxen in conditions of lead poisoning helps to reduce the concentration of xenobiotic in the bone tissue, which in turn leads to a decrease in the level of ionized calcium in the blood plasma, relative to the indices of the group of animals receiving xenobiotic alone. The weakening of the expression of the hemotoxic effect of lead in conditions of its prolonged intake into the organism of animals is confirmed by a decrease in the concentration of potassium in the blood plasma of animals receiving melaxen for therapeutic purposes. In addition to this, the effect of melaxen in the conditions of therapeutic use in lead poisoning helps restore the concentration of protein and sodium in the blood plasma of animals, relative to the indices of a group of rats treated with xenobiotic alone.

As a component of various enzymes, it refers to copper essential trace elements, but the excessive consumption of the metal leads to the development of the pathogenic effects of xenobiotics on the functional condition of the cardiovascular system. However, the works devoted to the study of the effectiveness of prophylactic calcium in a copper toxicity, is not in the current literature.The purpose:study the effect of long-term toxicity of copper on the functional state of the cardiovascular system and its reactivity in experimental hypercalcemia.Methods:Experimental hypercalcemia model was created by forming a pilot hypervitaminosis D, by introducing «Akvadetrim» atraumatic preparation through a probe into the stomach in the dose 3000 IU (0.2 ml) / 100 g of body weight for 30 days. Chronic copper poisoning model created by intragastric administration of copper sulfate solution at a dosage of 20 mg/kg (in terms of metal) for 30 days, daily one time a day. The study of the functional state of the cardiovascular system is to determine the mean arterial pressure, specific peripheral vascular resistance, stroke index, cardiac index, the reactivity of the renin-angiotensin system and adrenoreactivity cardiovascular system.Results:The experimental study revealed that long-term copper poisoning leads to the development of hypertension due to an increase in total peripheral vascular resistance, along with the marked decline in the pumping function of the heart. Experimental hypercalcemia simulated by intragastric administration of vitamin D promotes more pronounced toxic effects of copper sulfate on the cardiovascular system.Conclusion:Copper poisoning of the body is characterized by the development of hypertension and the condition of artificial hypercalcemia potentiates the cardiotoxic effects of copper.

Mercury and cadmium poisoning leads to the development of a powerful oxidative stress was associated with increased concentrations of malondialdehyde and hydroperoxide. These changes combined with a decrease in catalase activity, indicating that inhibition of the action of the antioxidant defense mechanisms of the system. Application melaxen in chronic intoxication with heavy metal salts, has a pronounced antioxidant effect, which leads to a reduction of lipid peroxidation and the simultaneous increase in the activity of catalase.

Chronic toxicity of copper sulfate leads to the formation of system hemodynamic disturbances, which manifests itself in the form of increased mean arterial pressure in experimental animals and reduction in the pumping function of the heart. Increased heart rate in experimental animals under conditions of chronic copper toxicity is compensatory in nature and is intended to maintain the level of cardiac output. The observed increase adrenal reactivity of cardiovascular system in animals receiving only insulated copper sulfate, apparently due to changes in the activity of sympathetic nervous system. Under the conditions of experimental hypercalcemia toxic effects of copper on the cardiovascular system become more pronounced, probably due to an increase in the absorption of the metal in gastrointestinal tract. Copper sulphate amid intragastric administration of vitamin D3 leads to greater inhibition of the contractile function of the heart, as compared with the group of animals treated only xenobiotic. Despite a significant reduction in cardiac index, formed pronounced arterial hypertension associated with a strong increase of the specific peripheral vascular resistance. Effect of copper sulfate adrenal reactivity cardiovascular system is more pronounced in animals with experimental hypercalcemia model.

Chronic toxicity of copper sulfate leads to the formation of system hemodynamic disturbances, which manifests itself in the form of increased mean arterial pressure in experimental animals and reduction in the pumping function of the heart. Increased heart rate in experimental animals under conditions of chronic copper toxicity is compensatory in nature and is intended to maintain the level of cardiac output. The observed increase adrenal reactivity of cardiovascular system in animals receiving only insulated copper sulfate, apparently due to changes in the activity of sympathetic nervous system. Under the conditions of experimental hypercalcemia toxic effects of copper on the cardiovascular system become more pronounced, probably due to an increase in the absorption of the metal in gastrointestinal tract. Copper sulphate amid intragastric administration of vitamin D3 leads to greater inhibition of the contractile function of the heart, as compared with the group of animals treated only xenobiotic. Despite a significant reduction in cardiac index, formed pronounced arterial hypertension associated with a strong increase of the specific peripheral vascular resistance. Effect of copper sulfate adrenal reactivity cardiovascular system is more pronounced in animals with experimental hypercalcemia model.

Under conditions of chronic cadmium intoxication leads to an increase in mean arterial pressure despite the simultaneous reduction of the contractile function of the heart. Under the experimental hypocalcemia toxic effects of cadmium on the cardiovascular system become more pronounced, which is manifested in even greater inhibition of pump function, which leads to a decrease in mean arterial pressure

The toxic effects of mercury results in the formation of pathologies of the cardiovascular system and the kidneys. Hemodynamic effect of xenobiotic has a pronounced hypertensive orientation, combined with a sharp decline in myocardial contractility. Changes in renal function in mercury poisoning manifested as increased diuresis and forming proteinuria. Melaxen application as a prophylactic agent in mercury intoxication virtually eliminates the toxic effects of pollutants, which is characterized by less severe disorders of the functional state of the cardiovascular system and the kidneys.

Chronic cadmium intoxication promotes marked changes in the functional state of the cardiovascular system. Cardiotoxic effects of cadmium is a hypertensive hemodynamics. Being a powerful pro-oxidants, cadmium activates lipid peroxidation and inhibits the activity of catalase. Application melaxen helps prevent cardiotoxic action of cadmium, which is confirmed by hemodynamic studies of the cardiovascular system. With its strong antioxidant properties, melaxen in cadmium poisoning reduces the activity of lipid peroxidation.

Chronic lead intoxication leads to increased mean arterial pressure despite the decline in stroke and cardiac index. Emerging hypertensive reaction in chronic lead poisoning caused by increase in the proportion of peripheral vascular resistance. The toxic effects of lead on the cardiovascular system in experimental hypocalcemia leads to a more pronounced disturbances of myocardial contractility and is accompanied with an increase in α-adrenoreactivity and increased activity of the renin-angiotensin system.

The chronic mercury intoxication forms expressed by the functional and morphological changes of the liver. Application melaxen as a prophylactic agent in chronic poisoning reduces the xenobiotic hepatotoxicity, significantly supported by the data as a morphological and biochemical studies.