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Central neuroplasticity and decreased heart rate variability after particulate matter exposure in mice.

Pham H, Bonham AC, Pinkerton KE, Chen CY - Environ. Health Perspect. (2009)

Bottom Line: We also determined the effect of iron on PM-exposure-induced decrease in HRV.Iron-soot exposure had no significant effect on resting membrane potential but decreased spiking responses of the identified cardiac vagal neurons to depolarizations (p < 0.05).The decreased spiking response was accompanied with a higher minimal depolarizing current required to evoke spikes and a lower peak discharge frequency.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, University of California at Davis, One Shields Avenue, Davis, CA 95616, USA

ABSTRACT

Background: Epidemiologic studies show that exposure to fine particulate matter [aerodynamic diameter < or = 2.5 microm (PM(2.5))] increases the total daily cardiovascular mortality. Impaired cardiac autonomic function, which manifests as reduced heart rate variability (HRV), may be one of the underlying causes. However, the cellular mechanism(s) by which PM(2.5) exposure induces decreased HRV is not known.

Objectives: We tested the hypothesis that exposure to PM(2.5) impairs HRV by decreasing the excitability of the cardiac vagal neurons in the nucleus ambiguus. We also determined the effect of iron on PM-exposure-induced decrease in HRV.

Methods: We measured 24-hr HRV in time domains from electrocardiogram telemetry recordings obtained in conscious, freely moving mice after 3 days of exposure to PM(2.5) in the form of soot only or iron-soot. In parallel studies, we determined the intrinsic properties of identified cardiac vagal neurons, retrogradely labeled with a fluorescent dye applied to the sinoatrial node.

Results: Soot-only exposure decreased short-term HRV (root mean square of successive difference). With the addition of iron, all HRV parameters were significantly reduced. In nonexposed mice, vagal blockade significantly reduced all HRV parameters, suggesting that HRV is, in part, under vagal regulation in mice. Iron-soot exposure had no significant effect on resting membrane potential but decreased spiking responses of the identified cardiac vagal neurons to depolarizations (p < 0.05). The decreased spiking response was accompanied with a higher minimal depolarizing current required to evoke spikes and a lower peak discharge frequency.

Conclusions: The data suggest that PM-induced neuroplasticity of cardiac vagal neurons may be one mechanism contributing to the cardiovascular consequences associated with PM(2.5) exposure seen in humans.

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Related in: MedlinePlus

Example tachograms from individual mice after 3 days of exposure to FA (A) or PM in the form of iron-soot (B).
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f2-ehp-117-1448: Example tachograms from individual mice after 3 days of exposure to FA (A) or PM in the form of iron-soot (B).

Mentions: Exposure to PM2.5 for 3 days reduced measures of HRV in C57BL/6 mice. A representative tachogram from an FA-exposed control mouse and an iron-soot–exposed mouse recorded during the first 24 hr after 3 days of exposure are shown in Figure 2. The PM2.5-exposed mouse (Figure 2B) showed reduced HRV, as indicated by less frequent and lower magnitude “fluctuations” in the RR intervals.


Central neuroplasticity and decreased heart rate variability after particulate matter exposure in mice.

Pham H, Bonham AC, Pinkerton KE, Chen CY - Environ. Health Perspect. (2009)

Example tachograms from individual mice after 3 days of exposure to FA (A) or PM in the form of iron-soot (B).
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2737024&req=5

f2-ehp-117-1448: Example tachograms from individual mice after 3 days of exposure to FA (A) or PM in the form of iron-soot (B).
Mentions: Exposure to PM2.5 for 3 days reduced measures of HRV in C57BL/6 mice. A representative tachogram from an FA-exposed control mouse and an iron-soot–exposed mouse recorded during the first 24 hr after 3 days of exposure are shown in Figure 2. The PM2.5-exposed mouse (Figure 2B) showed reduced HRV, as indicated by less frequent and lower magnitude “fluctuations” in the RR intervals.

Bottom Line: We also determined the effect of iron on PM-exposure-induced decrease in HRV.Iron-soot exposure had no significant effect on resting membrane potential but decreased spiking responses of the identified cardiac vagal neurons to depolarizations (p < 0.05).The decreased spiking response was accompanied with a higher minimal depolarizing current required to evoke spikes and a lower peak discharge frequency.

View Article: PubMed Central - PubMed

Affiliation: Department of Pharmacology, University of California at Davis, One Shields Avenue, Davis, CA 95616, USA

ABSTRACT

Background: Epidemiologic studies show that exposure to fine particulate matter [aerodynamic diameter < or = 2.5 microm (PM(2.5))] increases the total daily cardiovascular mortality. Impaired cardiac autonomic function, which manifests as reduced heart rate variability (HRV), may be one of the underlying causes. However, the cellular mechanism(s) by which PM(2.5) exposure induces decreased HRV is not known.

Objectives: We tested the hypothesis that exposure to PM(2.5) impairs HRV by decreasing the excitability of the cardiac vagal neurons in the nucleus ambiguus. We also determined the effect of iron on PM-exposure-induced decrease in HRV.

Methods: We measured 24-hr HRV in time domains from electrocardiogram telemetry recordings obtained in conscious, freely moving mice after 3 days of exposure to PM(2.5) in the form of soot only or iron-soot. In parallel studies, we determined the intrinsic properties of identified cardiac vagal neurons, retrogradely labeled with a fluorescent dye applied to the sinoatrial node.

Results: Soot-only exposure decreased short-term HRV (root mean square of successive difference). With the addition of iron, all HRV parameters were significantly reduced. In nonexposed mice, vagal blockade significantly reduced all HRV parameters, suggesting that HRV is, in part, under vagal regulation in mice. Iron-soot exposure had no significant effect on resting membrane potential but decreased spiking responses of the identified cardiac vagal neurons to depolarizations (p < 0.05). The decreased spiking response was accompanied with a higher minimal depolarizing current required to evoke spikes and a lower peak discharge frequency.

Conclusions: The data suggest that PM-induced neuroplasticity of cardiac vagal neurons may be one mechanism contributing to the cardiovascular consequences associated with PM(2.5) exposure seen in humans.

Show MeSH
Related in: MedlinePlus