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HERO ID
2435991
Reference Type
Journal Article
Subtype
Abstract
Title
Differential ventricular hemodynamic responses to particulate matter (PM) or ozone (O3)
Author(s)
Abston, ED; Sborz, N; Weiss, R; Champion, H; Tankersley, CG
Year
2010
Is Peer Reviewed?
Yes
Journal
American Journal of Respiratory and Critical Care Medicine
ISSN:
1073-449X
EISSN:
1535-4970
Volume
181
Page Numbers
A1722
Language
English
DOI
10.1164/ajrccm-conference.2010.181.1_MeetingAbstracts.A1722
Web of Science Id
WOS:000208771000722
Relationship(s)
is part of a larger document
3452678
Proceedings of the American Thoracic Society 2010 International Conference, May 14-19, 2010, New Orleans
Abstract
RATIONALE: Recent epidemiological studies show a link between adverse cardiovascular outcomes and increased levels of both PM and gaseous pollutants, including O3. Although previous work has thoroughly characterized many differential effects of PM and O3 in the lung, work exploring the effects of pollution on the heart thus far has focused on non invasive measures such as EKG and blood pressure. This experiment represents the first attempt at invasively quantifying and comparing the effects of O3 and PM on ventricular function using the pressure-volume relationship. The purpose of the current study is to determine whether or not exposure to PM or O3 causes differential ventricular hemodynamic responses in mice.
METHODS: C57BL/6J (B6) mice (n = 8-12) were exposed to either room air (RA), carbon black (CB, 0.55 mg/m^3) or O3 (0.5 ppm) for 3 hrs on 3 consecutive days. Approximately, 6-12 hrs after exposure on day 3, ventricular hemodynamic function was assessed in the left (LV) and right ventricle (RV) using a pressure-volume conductance catheter.
RESULTS: Following either RA, CB or O3 exposure, heart rate was similar among groups with an average of 591 bpm (see Table 1). With respect to LV function, exposure to CB induced a 19% decrease in cardiac output (Q) and O3 exposure led to a drop of 29% relative to RA exposure. The LV contractility index was decreased by 16% with CB, but remained unaffected after O3 exposure. The RV and LV pressures developed during contraction were unaffected by CB; however, O3 exposure increased RV pressure by 11%. Ejection fraction was decreased by 20% after CB exposure, but unchanged following O3.
CONCLUSION: While both CB and O3 significantly alter heart function separately, the ways in which the heart responds to the effects of either pollutant are quite different. The CB-induced decrease in Q accompanies a decrease in contractility and a lower ejection fraction. The O3-induced decrease in Q occurs with concomitant increases in RV pressure and pulmonary vascular resistance, which ultimately impede blood flow. Supported by NIEHS Training Grant # ES 07141 and by AG-21057.
Conference Name
American Thoracic Society 2010 International Conference
Conference Location
New Orleans, LA
Conference Dates
May 14-19, 2010
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