Key result
PM2.5 or silica exposure triggers delayed bradycardia and reduces HRV in a cardiovascular mouse model.
Why the study?
Does exposure to Seattle particulate matter (PM2.5) or silica reduce heart-rate variability in an apolipoprotein E knockout mouse model of cardiovascular disease?
Does exposure to Seattle particulate matter (PM2.5) or silica reduce heart-rate variability in an apolipoprotein E knockout mouse model of cardiovascular disease?
Exposure to ambient particulate matter (PM2.5) decreases heart rate variability and parasympathetic tone in a mouse model of cardiovascular disease, potentially increasing the risk of cardiac arrhythmias.
Answers are grounded in this paper and cite their sources.
May elevate arrhythmia risk in CVD patients; leaves open translation from this mouse model to humans.
Epidemiological studies show that the elderly and/or people with preexisting cardiovascular disease (CVD) are more susceptible to the adverse effects of ambient air pollution. Heart-rate variability (HRV) measured through electrocardiogram (ECG) is a sensitive and effective tool for monitoring the adverse effects of particulate matter (PM). Common HRV parameters used include the standard deviation of the interval between normal beats (SDNN), square root of the mean of the squared differences between normal beats (rMSSD), and distinct high, low, and very low components of frequency. Aged apolipoprotein E knockout transgenic mice, a model of CVD, were implanted with miniaturized ECG telemetry devices and intranasally exposed to saline, 50 microg Seattle PM(2.5) (PM having a mean aerodynamic diameter of < or = 2.5 microm), or silica. They were monitored for a 1-d baseline prior to and for 4 d following exposure. After an initial increase in both heart rate and activity in all groups, there was delayed bradycardia with no change in activity of the animals in the PM- and silica-exposed groups. In addition, with PM and silica exposure there was a decrease in HRV parameters, suggesting a decrease in parasympathetic tone, which may lead to cardiac arrhythmia and mortality. Seattle PM is a toxic species that modulates the autonomic nervous system in a mouse model of CVD.
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Corey et al. (2006) studied Cardiovascular disease model. Seattle PM(2.5) or silica vs. Saline was evaluated on Heart rate and heart-rate variability (HRV) parameters. Intranasal exposure to 50 microg Seattle PM2.5 or silica in a mouse model of cardiovascular disease caused delayed bradycardia and decreased heart-rate variability parameters.
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