Toxic effects of palladium compounds on the isolated rat heart

Abstract

Taken into consideration limited data about effects of palladium on cardiovascular system, the aim of our study was to compare toxicity of inorganic and organic palladium compounds on the isolated rat heart. The hearts (total number n=30, 6 for each experimental group) excised from Wistar albino rats, male sex, age 8 weeks, and body mass 180-200 g, were retrogradely perfused according to the Langendorff technique at constant perfusion pressure (70 cm H 2O). After the insertion of sensor in the left ventricle, the parameters of heart function: maximum rate of left ventricular pressure development (dP/dt max), systolic left ventricular pressure (SLVP), diastolic left ventricular pressure (DLVP), mean blood pressure (MBP) and heart rate (HR)), were continuously registered. The experiments were performed during control conditions, and in the presence of perfusion with incresing concentration of the following: (triethanolamine (TEA), triethanolamine acetate (TEAA), palladium(II)chloride (PdCl 2), and trans- dichlorobis(triethanolamine-N)palladium(II) complex (trans-[PdCl 2(TEA)2])) started every 30 minutes (30, 60, 90, 120 minute). dP/dt max was not affected significantly by either TEAA, TEA, PdCl 2 or Pd complex. SLVP was, also, not affected significantly by either TEAA, TEA, PdCl 2, or Pd complex. DLVP was significantly decreased by both TEAA and PdCl 2, while TEA and Pd complex did not show significant effect. MBP was significantly decreased only by PdCl 2, while TEAA, TEA and Pd complex did not show significant effect. HR was significantly decreased by all compounds- PdCl 2, TEAA, TEA and Pd complex. In our study, inorganic palladium compound (PdCl 2) induced clear depression of the isolated rat heart contractility, manifested as drop in diastolic and mean blood pressure , and as decrease of the heart rate. On the other hand, it seems that palladium, when bound in an organic compound (linked to TEA in Pd complex), does not contribute significantly to cardio-toxicity in our experimental conditions. © 2012 Bentham Science Publishers.