Original ArticleEvaluation of vascular tone and cardiac contractility in response to silver nanoparticles, using Langendorff rat heart preparation

Silver nanoparticles (AgNPs) have been widely used because of their antimicrobial properties. However, several reports suggest that AgNPs exposure promote cardiac effects that involve nitric oxide (NO) and oxidative stress (OS). Nevertheless, there are no studies related to AgNPs-induced effects in cardiac physiology. The aim of this study was to evaluate the AgNPs direct actions on coronary vascular tone and cardiac contractility using Langendorff rat heart preparation. Low concentrations of AgNPs (0.1 and 1 μg/mL) increased NO derived from inducible NO-synthase (iNOS), without modifying cardiac parameters. Meanwhile, high concentrations (10 and 100 μg/mL) promoted a sustained vasoconstriction and increased cardiac contractility related to OS, leading to rhabdomyolysis. Furthermore, AgNPs were internalized in the cardiac muscle, hindering classic actions induced by phenylephrine (Phe) and acetylcholine (ACh). These data suggest that AgNPs affect cardiac physiology in function of the concentration and in part of the NO generation, NOS expression and OS.

Graphical AbstractSilver nanoparticles (AgNPs) cardiac effects were evaluated using the Langendorff rat heart preparation. At low concentrations, AgNPs increased nitric oxide (NO) derived from inducible NO synthase (iNOS), without modifying coronary vascular tone nor cardiac contractility. Meanwhile, high concentrations induced a sustained vasoconstriction and increased cardiac contractility related to increased reactive oxygen species (ROS) levels, leading the triggering of rhabdomyolysis, which is the degradation of muscle. Furthermore, AgNPs were able to internalize to cardiac muscle cells, hindering the well-known actions induced by vasoactive controls phenylephrine (Phe) and acetylcholine (ACh). Future approaches are needed to elucidate the mechanism of action involved.304