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Oxidative Medicine and Cellular Longevity
Volume 2013, Article ID 901239, 10 pages
http://dx.doi.org/10.1155/2013/901239
Research Article

The Influence of Nrf2 on Cardiac Responses to Environmental Stressors

1Laboratory of Systems Physiology, Department of Kinesiology, University of North Carolina at Charlotte, Charlotte, NC, USA
2Laboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA
3Comparative Medicine Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA
4Division of Laboratory Animal Resources, Duke University Medical Center, Durham, NC, USA
5United States Environmental Protection Agency, Research Triangle Park, NC, USA

Received 11 January 2013; Accepted 26 March 2013

Academic Editor: Jingbo Pi

Copyright © 2013 Reuben Howden et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Nrf2 protects the lung from adverse responses to oxidants, including 100% oxygen (hyperoxia) and airborne pollutants like particulate matter (PM) exposure, but the role of Nrf2 on heart rate (HR) and heart rate variability (HRV) responses is not known. We hypothesized that genetic disruption of Nrf2 would exacerbate murine HR and HRV responses to severe hyperoxia or moderate PM exposures. and mice were instrumented for continuous ECG recording to calculate HR and HRV (low frequency (LF), high frequency (HF), and total power (TP)). Mice were then either exposed to hyperoxia for up to 72 hrs or aspirated with ultrafine PM (UF-PM). Compared to respective controls, UF-PM induced significantly greater effects on HR ( ) and HF HRV ( ) in mice compared to mice. mice tolerated hyperoxia significantly less than mice ( 22 hrs; ). Reductions in HR, LF, HF, and TP HRV were also significantly greater in compared to mice ( ). Results demonstrate that Nrf2 deletion increases susceptibility to change in HR and HRV responses to environmental stressors and suggest potential therapeutic strategies to prevent cardiovascular alterations.