Central Neuroplasticity and Decreased Heart Rate Variability after Particulate Matter Exposure in Mice

Abstract

BackgroundEpidemiologic studies show that exposure to fine particulate matter [aerodynamic diameter ≤ 2.5 μm (PM2.5)] 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 PM2.5 exposure induces decreased HRV is not known.ObjectivesWe tested the hypothesis that exposure to PM2.5 impairs HRV by decreasing the excitability of the cardiac vagal neurons in the nucleus ambiguus. We also detemined the effect of iron on PM-exposure–induced decrease in HRV.MethodsWe measured 24-hr HRV in time domains from electrocardiogram telemetry recordings obtained in conscious, freely moving mice after 3 days of exposure to PM2.5 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.ResultsSoot-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.ConclusionsThe data suggest that PM-induced neuroplasticity of cardiac vagal neurons may be one mechanism contributing to the cardiovascular consequences associated with PM2.5 exposure seen in humans.

Cardiopulmonary responses in spontaneously hypertensive and Wistar-Kyoto rats exposed to concentrated ambient particles from Detroit, Michigan

“…This is consistent with the bulk of the both the epidemiological (e.g., Devlin et al, 2003) and toxicological (e.g., Chen and Hwang, 2005) literature, which reports lower HRV parameters associated with PM exposure. Furthermore, the 2-3-ms difference in SDNN between CAPs-and air-exposed SH rats is similar to exposure-related changes in rodents from other PM studies that were found to be statistically significant (Pham et al, 2009;Chang et al, 2007). We suspect that with more animals per group (presently n = 4) that differences in HRV would also have been significant in this study.…”

A new cue for torpor induction: charcoal, ash and smoke

“…Importantly, our study identifies a charcoal and ash substrate as a new cue that signals antechinus to enhance torpor use to save energy. In rats and mice, exposure to particulate matter, such as ash, results in reduced heart rate or heart rate variability via vagal regulation and also causes lung inflammation (Swoap et al, 2008;Pham et al, 2009;Farraj et al, 2011). Additionally, as T b regulation involves the hypothalamus (Heller et al, 1977;Seebacher, 2009), a fast adjustment to the thermal physiology of the animal can be made, as the presence of these products of fire will herald a potential reduction in food availability.…”

Adverse Effects of Cigarette and Noncigarette Smoke Exposure on the Autonomic Nervous System

“…Nicotine in tobacco smoke stimulates nicotinic receptors in the rostral ventrolateral medulla, and decreases nitric oxide production centrally, thereby increasing central sympathetic outflow. Baroreflex suppression of sympathetic activation is attenuated in habitual smokers by 3 potential mechanisms: 1) neuroplasticity (PM 2.5 in tobacco smoke may induce neuroplasticity in the nucleus tractus solitarius, the first synapse of the baroreceptor afferents, thereby directly altering baroreflex responsiveness in smokers[34,35]); 2) oxidative stress (cigarette smoke, through particulate matter and/or nicotine, is known to generate oxidative stress[3]; in animal models, free radicals attenuated baroreceptor activity, while oxyradical scavengers increased baroreceptor activity[36,37]); and 3) endothelial dysfunction (chronic active and passive tobacco exposure is associated with increased vascular stiffness; vascular reactivity mediated by nitric oxide is impaired[38,39]; thus, blood pressure fluctuations transmitted to the baroreceptors through changes in stretch of the vascular wall are dampened). NO ¼ nitric oxide; ROS ¼ reactive oxygen species; SNS ¼ LUNG AFFERENT C-FIBERS.…”