Abstract

Increases in the concentration of airborne fine particles (< 0.1 µm, UFP) are positively correlated with increased cardiovascular mortality. UFP produced by the combustion of fossil fuels and wastes contain stable free radicals capable of redox cycling and producing oxidative stress. After inhalation, UFP transit from the lung to the heart raising the possibility that UFP produces oxidative stress in the heart by a direct action. This study determined whether radical‐containing UFP produce oxidative stress and contractile deficits in ALVM. Rat ALVM were treated with SiCuO UFP containing dichlorobenzene (DCB230, 8.8 and 17.6 µg/cm2) for 24 hr. DCB230 increased ROS production (measured by dihydroethidium staining) in ALVM by 50% relative to control. The higher dose killed all the cells. An IonOPtix system was used to assess contractile function in treated and control ALVM. Compared to control, DCB230‐treated ALVM showed decreased sarcomere length shortening percent and decreased the maximal velocities of shortening and re‐lengthening during stimulation (1Hz). In conclusion, treatment with UFP directly increased ROS production and decreased contractile function in ALVM. Support RR018766

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