Inhaled ambient-level traffic-derived particulates decrease cardiac vagal influence and baroreflexes and increase arrhythmia in a rat model of metabolic syndrome

Abstract

BackgroundEpidemiological studies have linked exposures to ambient fine particulate matter (PM2.5) and traffic with autonomic nervous system imbalance (ANS) and cardiac pathophysiology, especially in individuals with preexisting disease. It is unclear whether metabolic syndrome (MetS) increases susceptibility to the effects of PM2.5. We hypothesized that exposure to traffic-derived primary and secondary organic aerosols (P + SOA) at ambient levels would cause autonomic and cardiovascular dysfunction in rats exhibiting features of MetS. Male Sprague Dawley (SD) rats were fed a high-fructose diet (HFrD) to induce MetS, and exposed to P + SOA (20.4 ± 0.9 μg/m3) for 12 days with time-matched comparison to filtered-air (FA) exposed MetS rats; normal diet (ND) SD rats were separately exposed to FA or P + SOA (56.3 ± 1.2 μg/m3).ResultsIn MetS rats, P + SOA exposure decreased HRV, QTc, PR, and expiratory time overall (mean effect across the entirety of exposure), increased breathing rate overall, decreased baroreflex sensitivity (BRS) on three exposure days, and increased spontaneous atrioventricular (AV) block Mobitz Type II arrhythmia on exposure day 4 relative to FA-exposed animals receiving the same diet. Among ND rats, P + SOA decreased HRV only on day 1 and did not significantly alter BRS despite overall hypertensive responses relative to FA. Correlations between HRV, ECG, BRS, and breathing parameters suggested a role for autonomic imbalance in the pathophysiologic effects of P + SOA among MetS rats. Autonomic cardiovascular responses to P + SOA at ambient PM2.5 levels were pronounced among MetS rats and indicated blunted vagal influence over cardiovascular physiology.ConclusionsResults support epidemiologic findings that MetS increases susceptibility to the adverse cardiac effects of ambient-level PM2.5, potentially through ANS imbalance.Electronic supplementary materialThe online version of this article (doi:10.1186/s12989-017-0196-2) contains supplementary material, which is available to authorized users.

Inhalation of printer-emitted particles impairs cardiac conduction, hemodynamics, and autonomic regulation and induces arrhythmia and electrical remodeling in rats

“…The concomitant pressure increase with a restoration of BRS slope suggests PEPs restored BRS at a higher mean systolic pressure through 'baroreflex resetting' [85]. We previously found in rats with metabolic syndrome that traffic PM simultaneously decreased BRS and HRV, with equivalent effects on BRS (− 0.3 ms/mmHg) and similar correlations between BRS and HRV as found here [86]. Thus, similar to other PM, PEPs exposure likely promotes hypertension not only through autonomic imbalance but also via impaired baroreflexes.…”

“…Likewise, PEPs increased spontaneous ventricular premature beats at both 2 days and 5 weeks after the 21-day exposure, complementing epidemiologic associations between PM exposure and spontaneous ventricular arrhythmia [81,[88][89][90][91] and sudden cardiac arrest [92,93]. Interestingly, aerosol exposures in noninvasive rat models of CVD typically provoke spontaneous atrioventricular block arrhythmias [45,86,[94][95][96][97][98], which differ from the premature ventricular ectopy that predominates with PM exposure in humans. Yet, rodent models of surgical myocardial infarction [99][100][101] or genetic dilated fibrotic cardiomyopathy [102] have more consistently demonstrated tachyarrhythmias with PM exposures.…”

“…ECG waveforms were analyzed with ecgAuto, v3.3 (Emka Technologies, Paris, France) for mean RR intervals, HRV, and arrhythmia as we have previously described [86,94]. A library of 224 manually marked representative PQRST complexes was used to identify beat landmarks for ECG analyses according to previously described criteria [86]. ECG analyses were performed on all 4 BL days, inhalation exposure days 1, 9, and 21, and all three stress test days.…”

“…We excluded arrhythmias (> 18% reduction or > 25% increase in RR relative to the average of the prior 4 RRs) and, on select days, identified and quantified them as previously described [86] while blind to treatment and with verification by examination of concurrent LVP waveforms. ECG waveforms were analyzed in 5-min segments continuously over all BL days, select exposure days (1,5,9,13,17,20,21), a recovery day (day 22), and all stress test days.…”

“…ECG waveforms were analyzed in 5-min segments continuously over all BL days, select exposure days (1,5,9,13,17,20,21), a recovery day (day 22), and all stress test days. HRV analyses generated the timedomain variables SDNN and RMSSD, as well as the frequency-domain variables, HF (0.75-3.50 Hz), LF (0.20-0.75 Hz), and their ratio (LF/HF) as previously described [86,94].…”