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Acrolein inhalation causes myocardial strain delay and decreased cardiac performance as detected by high-frequency echocardiography in mice
Citation:
Thompson, L., A. Ledbetter, N. Coates, W. Cascio, M. Hazari, AND A. Farraj. Acrolein inhalation causes myocardial strain delay and decreased cardiac performance as detected by high-frequency echocardiography in mice. Society of Toxicology, San Dieego, CA, March 22 - 26, 2015.
Impact/Purpose:
This abstract describes novel cardiovascular findings with exposure to a component of air pollution using an in vivo ultrasound imaging system that provides detailed assessment of cardiac and vascular function. This system enables noninvasive acquisition of precise and reproducible functional endpoints. This approach may improve the accuracy and reliability of hazard and mode of action determinations, may help reduce uncertainty in risk assessment.
Description:
Acrolein, an unsaturated aldehyde found in air pollution, impairs Ca2+ flux and contraction in cardiomyocytes in vitro. To better define direct and delayed functional cardiac effects, we hypothesized that a single exposure to acrolein would modify myocardial strain and performance in vivo. Male C57Bl/6J mice were exposed once to filtered air (FA) or acrolein (0.3 or 3 ppm) for 3 hr in whole body plethysmography chambers (n=6). High-frequency echocardiographic data (HF Echo) was collected at 40 MHz with a Vevo2100 ultrasound/MS550D transducer one day before and 1 and 24 hr post-exposure. Parasternal short axis views were collected for myocardial strain analysis of the left ventricular lateral and anterior free walls. Apical views were taken to assess myocardial performance index (MPI) using pulse wave Doppler of transmitral flow. Exposure to 3 ppm acrolein delayed peak circumferential strain (reported as % cardiac cycle), an indicator of cardiac dyssynchrony, at 1 hr (10.1 ± 2.4%, p=0.01) and 24 hr (8.2 ± 0.9%, p=0.05) post-exposure compared to pre-exposure (3.5 ± 1.1%) and respective FA time-points (4.9 ± 1.4% and 2.9 ± 0.7%, both p=0.04). Peak myocardial strain was unaltered with 0.3 acrolein but MPI increased, indicating decreased cardiac performance, at 1 hr (0.40 ± 0.02, p=0.01) and 24 hr (0.39 ± 0.03, p=0.02) post-exposure compared to pre-exposure (0.31 ± 0.02) and FA 1 hr post-exposure (0.33 ± 0.03, p=0.04). MPI also increased with 3 ppm acrolein 24 hrs post-exposure (0.38 ± 0.01 vs. pre-exposure at 0.33 ± 0.01, p=0.1). M-mode, pulmonary artery flow and breathing parameter data are currently being analyzed. We conclude from these data that even acute low level inhalation of acrolein can modify cardiac function and cause latent effects; as such, HF Echo appears to be a sensitive tool for investigating cardiovascular responses to air pollutants (This abstract does not reflect EPA policy).