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Introduction. One of the risk factors for cardiovascular diseases is the toxic metal pollution of the industrial area and the environment. Lead is the most critical of toxic metals. In industrial conditions, the body’s exposure to harmful substances is often combined with muscular work of varying severity. It has not been studied enough how these combinations influence the development of pathological processes associated with harmful exposure. Materials and methods. The subchronic experiment was carried out on white outbred male rats for six weeks. Intoxication was simulated by repeated intraperitoneal injections of lead acetate three times a week. Running was chosen to model the muscle exercise at a 25 m/min speed for 10 minutes 5 days a week. We performed biochemical and electrocardiographic studies. Blood pressure parameters were recorded. Muscle contractility was studied on isolated multicellular preparations of the right ventricular myocardium in isometric and physiological contraction modes. The ratio of myosin heavy chains was determined by the polyacrylamide gel electrophoresis. The sliding velocity of reconstituted thin filaments on myosin using an in vitro motility assay. Results. Physical exercise under lead intoxication normalized the level of calcium and the angiotensin-converting enzyme activity in the blood serum, the voltage of the isoelectric line and the amplitude of the T wave on the electrocardiogram. The combined action of lead and physical exercise showed an increase in the creatinine kinase-MB level. We found that the effect of exercise under lead intoxication on myocardial contractility was ambiguous. The maximum isotonic shortening velocity in trabeculae was normalized, but the maximum rate of strength development in the isometric mode in the papillary muscles decreased to a greater extent than under lead intoxication. The maximum sliding velocity of reconstituted thin filaments and myosin and the heavy chain ratio was partly normalized. Conclusion. In general, muscle exercise attenuated the lead cardiotoxic effects.

Introduction. There is a high chance of a link between cardiovascular conditions and occupational or environmental exposure to lead. Taking into account the peculiarities of lead intoxication and the metal common occurrence it appeared to necessarily prove further experimental research of lead cardiotoxicity. Material and methods. After repeated intraperitoneal administration of sublethal doses of lead acetate to outbred male rats 3 times a week for 5 weeks, there was obtained the moderately pronounced subchronic lead intoxication manifested by some characteristic features. Cardiotoxic effects on myocardial contractility were studied by the analysis of the mechanical activity of isolated preparations of right ventricular trabeculae and papillary muscles contracting in isotonic and physiological modes of loading. Myocardial contractile function was also studied at the molecular level by measuring the sliding velocity of reconstructed thin filaments over myosin. Results. In papillary muscles lead intoxication led to a decrease in the maximal rate of isotonic shortening for all afterloads and a decrease in the thin filament sliding velocity in the in vitro motility assay. The same type of muscle from lead-exposed rats displayed marked changes in most of the main characteristics of afterload contraction-relaxation cycles, but in trabeculae, these changes were less pronounced. The reported changes were attenuated to some extent in rats similarly exposed to lead while being treated with a Ca-containing bio protector. The amount of work produced by both muscle preparations was unchanged under lead intoxication over the entire range of afterloads, which is an evidence of adaptation to the production of adequate mechanical work despite resulting contractility disturbances. Conclusions. 1. Subchronic lead intoxication was shown to cause contractile dysfunction of rat myocardium. In papillary muscles the alterations were observed more than in trabeculae. The changes in contractile proteins corresponded with those seen in myocardium structures. 2. The reported changes were attenuated to some extent in rats being treated with a Ca-containing bio protector.