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

Inhaled ambient-level traffic-derived particulates decrease cardiac vagal influence and baroreflexes and increase arrhythmia in a rat model of metabolic syndrome - Descarga este documento en PDF. Documentación en PDF para descargar gratis. Disponible también para leer online.

Particle and Fibre Toxicology

, 14:16

First Online: 25 May 2017Received: 02 November 2016Accepted: 15 May 2017DOI: 10.1186-s12989-017-0196-2

Cite this article as: Carll, A.P., Crespo, S.M., Filho, M.S. et al. Part Fibre Toxicol 2017 14: 16. doi:10.1186-s12989-017-0196-2


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-m 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-m.

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.

KeywordsParticulate matter Secondary organic aerosol Baroreflex Heart rate variability Autonomic Arrhythmia Traffic Respiratory Cardiopulmonary AbbreviationsANSautonomic nervous system

APBatrial premature beat


BPblood pressure

BPMbeats per minute

BRSbaroreflex sensitivity

CAPsconcentrated ambient particulates

CMDcount median diameter

COcarbon monoxide

CPCcondensation particle counter

CVcoefficient of variation

dP-dtmaxmaximum rate of increase in aortic pressure per beat


Frespiratory frequency

FAfiltered air

HFhigh frequency power spectral HRV

HFrDhigh fructose diet

HRVheart rate variability

LFlow frequency power spectral HRV

MetSmetabolic syndrome

MMDmass median diameter


NDnormal diet

NOnitric oxide

NOxnitrogen oxides


P + SOAprimary and secondary organic aerosols

PM2.5particulate matter <2.5 um in diameter

PPpulse pressure

RMSSDroot mean squared of successive differences

SDSprague Dawley

SDNNstandard deviation of normal interbeat intervals

SEstandard error

SMPSscanning mobility particle sizer

TEexpiratory time

TIinspiratory time

TTtotal respiratory cycle time

Electronic supplementary materialThe online version of this article doi:10.1186-s12989-017-0196-2 contains supplementary material, which is available to authorized users.

Autor: Alex P. Carll - Samir M. Crespo - Mauricio S. Filho - Douglas H. Zati - Brent A. Coull - Edgar A. Diaz - Rodrigo D. 


Documentos relacionados