Abstract
Because epidemiology studies consistently identify the elderly at risk for air pollution-related morbidity and mortality, we developed a model of senescent-dependent susceptibility based on indices of physiological aging. In the current study, we hypothesized that heart-rate regulation during particulate matter (PM) exposure differs with senescence-dependent susceptibility owing to variation in autonomic nervous control. Heart rate (HR) and heart-rate variability (HRV) parameters were measured from 162 samples of 2-min electrocardiograph (ECG) recordings in age-matched healthy (n = 5) and terminally senescent (n = 3) AKR mice during 3-h exposures to filtered-air (FA, day 1) and carbon black (CB, day 4; 3). On day 1, HR was significantly (p <.01) depressed during FA in terminally senescent mice. By day 4, HR was further slowed significantly (p <.01) due to the effects of CB exposure for 3 days. The combined effects of terminal senescence and CB exposure acted to depress HR to an average (±SEM) 445 ± 40 bpm, or ∼80 bpm lower compared to healthy HR responses. The change in rMSSD, an HRV parameter corresponding to relative influences of parasympathetic tone on HR, was significantly (p <.01) greater on day 1 and day 4 in terminally senescent mice compared to healthy mice. In contrast, the LF/HF ratio, an HRV parameter derived from spectral analysis indicating relative changes in cardiac sympathetic tone, was significantly (p <.01) depressed in terminally senescent mice on day 1. By day 4, significant increases in LF/HF were evident in healthy mice during CB exposure, suggesting that HR regulation was associated with an increase in sympathetic tone. Alternatively, terminally senescent mice appeared to modulate a lower HR without change in LF/HF ratio during CB exposure, suggesting an absence of sympathetic tone. In conclusion, older healthy mice increase cardiac sympathetic tone during PM exposure while terminally senescent mice show a greater PM-induced parasympathetic tone in regulating HR. The significance of the current results suggest that PM-induced HR regulatory changes may ultimately depend on the degree of physiological aging.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 381-390 |
| Number of pages | 10 |
| Journal | Inhalation Toxicology |
| Volume | 16 |
| Issue number | 6-7 |
| DOIs | |
| State | Published - Jun 2004 |
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ASJC Scopus subject areas
- Toxicology
- Health, Toxicology and Mutagenesis
Cite this
Particle effects on heart-rate regulation in senescent mice. / Tankersley, Clarke G.; Campen, Matthew; Bierman, Alexis; Flanders, Susan E.; Broman, Karl W.; Rabold, Richard.
In: Inhalation Toxicology, Vol. 16, No. 6-7, 06.2004, p. 381-390.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Particle effects on heart-rate regulation in senescent mice
AU - Tankersley, Clarke G.
AU - Campen, Matthew
AU - Bierman, Alexis
AU - Flanders, Susan E.
AU - Broman, Karl W.
AU - Rabold, Richard
PY - 2004/6
Y1 - 2004/6
N2 - Because epidemiology studies consistently identify the elderly at risk for air pollution-related morbidity and mortality, we developed a model of senescent-dependent susceptibility based on indices of physiological aging. In the current study, we hypothesized that heart-rate regulation during particulate matter (PM) exposure differs with senescence-dependent susceptibility owing to variation in autonomic nervous control. Heart rate (HR) and heart-rate variability (HRV) parameters were measured from 162 samples of 2-min electrocardiograph (ECG) recordings in age-matched healthy (n = 5) and terminally senescent (n = 3) AKR mice during 3-h exposures to filtered-air (FA, day 1) and carbon black (CB, day 4; 3). On day 1, HR was significantly (p <.01) depressed during FA in terminally senescent mice. By day 4, HR was further slowed significantly (p <.01) due to the effects of CB exposure for 3 days. The combined effects of terminal senescence and CB exposure acted to depress HR to an average (±SEM) 445 ± 40 bpm, or ∼80 bpm lower compared to healthy HR responses. The change in rMSSD, an HRV parameter corresponding to relative influences of parasympathetic tone on HR, was significantly (p <.01) greater on day 1 and day 4 in terminally senescent mice compared to healthy mice. In contrast, the LF/HF ratio, an HRV parameter derived from spectral analysis indicating relative changes in cardiac sympathetic tone, was significantly (p <.01) depressed in terminally senescent mice on day 1. By day 4, significant increases in LF/HF were evident in healthy mice during CB exposure, suggesting that HR regulation was associated with an increase in sympathetic tone. Alternatively, terminally senescent mice appeared to modulate a lower HR without change in LF/HF ratio during CB exposure, suggesting an absence of sympathetic tone. In conclusion, older healthy mice increase cardiac sympathetic tone during PM exposure while terminally senescent mice show a greater PM-induced parasympathetic tone in regulating HR. The significance of the current results suggest that PM-induced HR regulatory changes may ultimately depend on the degree of physiological aging.
AB - Because epidemiology studies consistently identify the elderly at risk for air pollution-related morbidity and mortality, we developed a model of senescent-dependent susceptibility based on indices of physiological aging. In the current study, we hypothesized that heart-rate regulation during particulate matter (PM) exposure differs with senescence-dependent susceptibility owing to variation in autonomic nervous control. Heart rate (HR) and heart-rate variability (HRV) parameters were measured from 162 samples of 2-min electrocardiograph (ECG) recordings in age-matched healthy (n = 5) and terminally senescent (n = 3) AKR mice during 3-h exposures to filtered-air (FA, day 1) and carbon black (CB, day 4; 3). On day 1, HR was significantly (p <.01) depressed during FA in terminally senescent mice. By day 4, HR was further slowed significantly (p <.01) due to the effects of CB exposure for 3 days. The combined effects of terminal senescence and CB exposure acted to depress HR to an average (±SEM) 445 ± 40 bpm, or ∼80 bpm lower compared to healthy HR responses. The change in rMSSD, an HRV parameter corresponding to relative influences of parasympathetic tone on HR, was significantly (p <.01) greater on day 1 and day 4 in terminally senescent mice compared to healthy mice. In contrast, the LF/HF ratio, an HRV parameter derived from spectral analysis indicating relative changes in cardiac sympathetic tone, was significantly (p <.01) depressed in terminally senescent mice on day 1. By day 4, significant increases in LF/HF were evident in healthy mice during CB exposure, suggesting that HR regulation was associated with an increase in sympathetic tone. Alternatively, terminally senescent mice appeared to modulate a lower HR without change in LF/HF ratio during CB exposure, suggesting an absence of sympathetic tone. In conclusion, older healthy mice increase cardiac sympathetic tone during PM exposure while terminally senescent mice show a greater PM-induced parasympathetic tone in regulating HR. The significance of the current results suggest that PM-induced HR regulatory changes may ultimately depend on the degree of physiological aging.
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U2 - 10.1080/08958370490439551
DO - 10.1080/08958370490439551
M3 - Article
VL - 16
SP - 381
EP - 390
JO - Inhalation Toxicology
JF - Inhalation Toxicology
SN - 0895-8378
IS - 6-7
ER -