Acrolein Inhalation Alters Myocardial Synchrony and Performance at and Below Exposure Concentration that Cause Ventilatory Responses in Mice
we examined the cardiovascular effects acrolein inhalation, particularly on myocardial synchrony and performance via ultrasound echocardiography. Male C57Bl/6J mice (n=6/group) were exposed to filtered air (FA), 0.3 ppm acrolein, or 3.0 ppm acrolein for 3 hours in whole body plethysmography chambers. Cardiac strain data, heart function, and transmitral blood flow were investigated with echocardiography (40 MHz) 1 day prior to exposure, 1 hour after exposure, and 1 day after exposure. During the first 30 minutes of exposure, breathing frequency decreased. tidal volume increased, and expiratory/inspiratory time ratio increased in response to 3.0 ppm acrolein. Elapsed time between peak strain in adjacent wall segments (i.e. myocardial strain delay), a measure of myocardial dyssynchrony, increased significantly in mice exposed to 3.0 ppm acrolein at 1 and 24 hours post-exposure. Mice exposed to 0.3 ppm acrolein did not demonstrate changes in myocardial synchrony but did show decreases in myocardial performance, i.e. increased Tei index, at both 1 and 24 hours post-exposure.
This dataset is associated with the following publication:
Thompson, L., A. Ledbetter , N. Coates , W. Cascio , M. Hazari , and A. Farraj. Acrolein inhalation alters myocardial synchrony and performance at and below exposure concentrations that cause ventilatory responses. Cardiovascular Toxicology. Humana Press Incorporated, Totowa, NJ, USA, 17(2): 97-108, (2017).
Complete Metadata
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| description | we examined the cardiovascular effects acrolein inhalation, particularly on myocardial synchrony and performance via ultrasound echocardiography. Male C57Bl/6J mice (n=6/group) were exposed to filtered air (FA), 0.3 ppm acrolein, or 3.0 ppm acrolein for 3 hours in whole body plethysmography chambers. Cardiac strain data, heart function, and transmitral blood flow were investigated with echocardiography (40 MHz) 1 day prior to exposure, 1 hour after exposure, and 1 day after exposure. During the first 30 minutes of exposure, breathing frequency decreased. tidal volume increased, and expiratory/inspiratory time ratio increased in response to 3.0 ppm acrolein. Elapsed time between peak strain in adjacent wall segments (i.e. myocardial strain delay), a measure of myocardial dyssynchrony, increased significantly in mice exposed to 3.0 ppm acrolein at 1 and 24 hours post-exposure. Mice exposed to 0.3 ppm acrolein did not demonstrate changes in myocardial synchrony but did show decreases in myocardial performance, i.e. increased Tei index, at both 1 and 24 hours post-exposure. This dataset is associated with the following publication: Thompson, L., A. Ledbetter , N. Coates , W. Cascio , M. Hazari , and A. Farraj. Acrolein inhalation alters myocardial synchrony and performance at and below exposure concentrations that cause ventilatory responses. Cardiovascular Toxicology. Humana Press Incorporated, Totowa, NJ, USA, 17(2): 97-108, (2017). |
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| identifier | https://doi.org/10.23719/1427298 |
| keyword |
[
"Ambient air quality",
"acrolein",
"air pollution",
"air quality",
"echocardiography",
"heart function",
"myocardial dyssynchrony",
"myocardial synchrony"
]
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| license | https://pasteur.epa.gov/license/sciencehub-license.html |
| modified | 2018-03-20 |
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"name": "U.S. EPA Office of Research and Development (ORD)",
"subOrganizationOf": {
"name": "U.S. Environmental Protection Agency",
"subOrganizationOf": {
"name": "U.S. Government"
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| references |
[
"https://doi.org/10.1007/s12012-016-9360-4"
]
|
| rights |
null
|
| title | Acrolein Inhalation Alters Myocardial Synchrony and Performance at and Below Exposure Concentration that Cause Ventilatory Responses in Mice |
