Limits...
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.

Show MeSH

Related in: MedlinePlus

Group data of 12-hr HRV in mice exposed to PM2.5 with (F–J) or without iron (A–E). All data are expressed as percent changes from the average values of the FA-exposed control group (mean ± SE).*p < 0.05 between the two time points.
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC2737024&req=5

f4-ehp-117-1448: Group data of 12-hr HRV in mice exposed to PM2.5 with (F–J) or without iron (A–E). All data are expressed as percent changes from the average values of the FA-exposed control group (mean ± SE).*p < 0.05 between the two time points.

Mentions: When effects were partitioned into dark and light postexposure periods, there was an overall soot-exposure–induced decrease in all measures of HRV (Figure 4A–E). The effects of PM2.5 exposure in the form of soot only were globally more prominent during the dark periods than during the light periods (Figure 4A–E). In addition, the decrease in HRV during the dark periods was greater on post exposure day 2 for overall HRV (Figure 4A), short-term HRV (Figure 4C), and HRV due to 2-min cycle length (Figure 4D), suggesting a lag time for the full effect of PM2.5 exposure.


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)

Group data of 12-hr HRV in mice exposed to PM2.5 with (F–J) or without iron (A–E). All data are expressed as percent changes from the average values of the FA-exposed control group (mean ± SE).*p < 0.05 between the two time points.
© Copyright Policy - public-domain
Related In: Results  -  Collection

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

f4-ehp-117-1448: Group data of 12-hr HRV in mice exposed to PM2.5 with (F–J) or without iron (A–E). All data are expressed as percent changes from the average values of the FA-exposed control group (mean ± SE).*p < 0.05 between the two time points.
Mentions: When effects were partitioned into dark and light postexposure periods, there was an overall soot-exposure–induced decrease in all measures of HRV (Figure 4A–E). The effects of PM2.5 exposure in the form of soot only were globally more prominent during the dark periods than during the light periods (Figure 4A–E). In addition, the decrease in HRV during the dark periods was greater on post exposure day 2 for overall HRV (Figure 4A), short-term HRV (Figure 4C), and HRV due to 2-min cycle length (Figure 4D), suggesting a lag time for the full effect of PM2.5 exposure.

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