Effects of Lead and/or Cadmium on the Contractile Function of the Rat Myocardium Following Subchronic Exposure and Its Attenuation with a Complex of Bioprotectors

Abstract

Background: As by-products of copper smelting, lead and cadmium pollute both workplace air at metallurgical plants and adjacent territories. Their increased levels in the human body pose a higher risk of cardiovascular diseases. The objective of our study was evaluate changes in the rat myocardium contractile function following moderate subchronic exposure to soluble lead and/or cadmium salts and its attenuation by means of a complex of bioprotectors. Materials and methods: The subchronic exposure of rats was modelled by intraperitoneal injections of 3-H2O lead acetate and/or 2.5-H2O cadmium chloride in single doses, 6.01 mg of Pb and 0.377 mg of Cd per kg of body weight, respectively, 3 times a week during 6 weeks. The myosin heavy chains isoform ratio was estimated by gel electrophoresis. Biomechanical measurements were performed on isolated multicellular preparations of the myocardium (trabeculae and papillary muscles) from the right ventricle. Results: The subchronic lead exposure slowed down the contraction and relaxation cycle and increased myosin expression towards slowly cycling V3 isomyosins. Cadmium intoxication, on the contrary, shortened the contraction and relaxation cycle and shifted the ratio of isomyosin forms towards rapidly cycling V1. Following the combined exposure to lead and cadmium, some contractile characteristics changed in the direction typical of the effect of lead while others – in that of cadmium. We observed that the metal combination either neutralized or enhanced the isolated damaging effect of each heavy metal. The use of a complex of bioprotectors normalized the myocardial contractility impaired by the exposure to lead and cadmium either partially or completely. Discussion: Despite the changes in myocardial contractility following the subchronic lead and cadmium exposure, the mechanisms of heterometric regulation were maintained. The adverse cardiotoxic effect of the combination of these industrial contaminants may be weakened by administering a complex of bioprotectors.