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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

Experimental protocols. (A) Reduced HRV induced by PM2.5 exposure. (B) Effects of autonomic blockers on HRV. (C) Reduced excitability of cardiac vagal neurons induced by PM2.5 exposure.
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f1-ehp-117-1448: Experimental protocols. (A) Reduced HRV induced by PM2.5 exposure. (B) Effects of autonomic blockers on HRV. (C) Reduced excitability of cardiac vagal neurons induced by PM2.5 exposure.

Mentions: As illustrated in Figure 1A, mice were exposed to FA or PM2.5 for 3 days (6 hr/day, 0900–1500 hours) 3 weeks after ECG telemetry device implant. Continuous ECG signals were recorded in freely moving mice for 48 hr after the last day of exposure (0800–1800 hours). The mice remained in their home cage throughout the exposure and recording period.


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)

Experimental protocols. (A) Reduced HRV induced by PM2.5 exposure. (B) Effects of autonomic blockers on HRV. (C) Reduced excitability of cardiac vagal neurons induced by PM2.5 exposure.
© Copyright Policy - public-domain
Related In: Results  -  Collection

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

f1-ehp-117-1448: Experimental protocols. (A) Reduced HRV induced by PM2.5 exposure. (B) Effects of autonomic blockers on HRV. (C) Reduced excitability of cardiac vagal neurons induced by PM2.5 exposure.
Mentions: As illustrated in Figure 1A, mice were exposed to FA or PM2.5 for 3 days (6 hr/day, 0900–1500 hours) 3 weeks after ECG telemetry device implant. Continuous ECG signals were recorded in freely moving mice for 48 hr after the last day of exposure (0800–1800 hours). The mice remained in their home cage throughout the exposure and recording period.

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