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Introduction A number of epidemiologic and experimental studies have demonstrated that cadmium exposure increases the risk of cardiovascular diseases. However, it has not been investigated so far whether the cardiotoxicity of cadmium ions and cadmium oxide nanoparticles are similar. Methods Subchronic cadmium poisoning was modelled on outbred white male rats by repeated intraperitoneal injections of cadmium chloride (CdCl 2 ) solution or cadmium oxide nanoparticles (CdO NPs) 3 times a week for 6 weeks. Single doses of Cd were 0.38 and 0.22 mg Cd per kg of body weight, respectively. Results In rats of both Cd-exposed groups were found signs of hepatotoxicity and nephrotoxicity accompanied by cardiotoxic effects manifested by changes in hemodynamic parameters and myocardial contractility. The force of contractions decreased while the muscle isometric contraction–relaxation cycle of isolated myocardial preparations shortened. The change in the maximum velocity of isotonic shortening of papillary muscles correlated with change in the content of α- or β-myosin heavy chains following the exposure to CdCl 2 or CdO NPs, respectively. In the NPs-exposed rats, the mechanical work performed by cardiac muscles was found to be decreased. Conclusions We established that moderate subchronic cadmium exposure weakened the pumping function of the heart due to the cardiotoxic effects at the cellular and molecular levels. At the same time, we observed not only quantitative, but also certain qualitative differences in the cardiotoxic effects of CdCl 2 and CdO NPs, probably associated with a more expressed oxidative stress induced by nanoparticles.

Subchronic intoxications induced in male rats by repeated intraperitoneal injections of lead acetate and cadmium chloride, administered either alone or in combination, are shown to affect the biochemical, cytological and morphometric parameters of blood, liver, heart and kidneys. The single twitch parameters of myocardial trabecular and papillary muscle preparations were measured in the isometric regime to identify changes in the heterometric (length-force) and chronoinotropic (frequency-force) contractility regulation systems. Differences in the responses of these systems in trabecules and papillary muscles to the above intoxications are shown. A number of myocardium mechanical characteristics changing in rats under the effect of a combined lead-cadmium intoxication and increased proportion of α-myosin heavy chains were observed to normalize fully or partially if such intoxication was induced against background administration of a proposed bioprotective complex. Based on the experimental results and literature data, some assumptions are suggested concerning the mechanisms of the cardiotoxic effects produced by lead and cadmium.