You are here:
Inhalation of Photochemically Altered Urban Mixtures Depresses Cardiac Function in Mice
Citation:
McIntosh-Kastrinsky, R., K. Sexton, C. Jania, S. Tilley, I. Jaspers, D. DIAZ SANCHEZ, M. I. GILMOUR, R. B. DEVLIN, W. CASCIO, AND H. TONG. Inhalation of Photochemically Altered Urban Mixtures Depresses Cardiac Function in Mice. Presented at American Thoracic Society (ATS) Annual meeting, San Francisco, CA, May 18 - 23, 2012.
Impact/Purpose:
This study demonstrated that acute smog exposure significantly decreases baseline LVDP and cardiac contractility in mice, indicating that photochemically altered urban air pollution worsens cardiac function
Description:
Rationale: Epidemiological studies have indicated an association between urban air pollution exposure and cardiovascular morbidity and mortality. The present study was designed to evaluate the cardiac effects of inhaled photochemical products in urban mixtures in a murine model. Methods: Four-month old mice were exposed to two concentrations of a photochemically aged Urban Mixtures (smog) or filtered air (FA) for 4 hours in an outdoor irradiation chamber. The Urban Mixture composition (50+ hydrocarbons) is based on EPA analyses of 40+ cities and was used to create two test mixtures ofdifferent concentrations but ofthe same composition of the primary organics. Smog-Group-2) had 50% more organics (3 ppmC) and 30% more NOx (0.37 ppm) than smog-group-l), but produced only slightly more ozone (0.34 and 0.33 ppm), while producing more secondary carbonyls. Eight hours after exposure cardiac effects were assessed by Langendorff-method of cardiac perfusion. Isolated mouse hearts were perfused for 25 min prior to 20 min of global ischemia followed by 2 hours of reperfusion. Left ventricular developed pressure (LVDP), heart rate, coronary artery flow rate, and cardiac contractility were measured at baseline and 60 min after reperfusion. Results: Hearts from the two smog-exposed groups had significantly lower baseline LVDP (69.2±16.0 cmH20 for smog-group-1 and 75.1±23.0 cmH20 for smog-group-2) compared to FA-group (146.4±14.8 cmH20; p<0.05). Baseline left ventricular contractility was also significantly depressed by the smog inhalation. The maximum +dp/dt was significantly lower in both smog groups (2764±558.8 cmH20/s for smog-group-1 and 2945±765.7 cmH20/s for smog-group-2) compared to FA group (5405±400.2 cmH20/s; p<0.05). In addition, the minimum -dp/dt was increased by the smog inhalation (-1822±335.5 cmH20/s for smog-group1
and -2070±625.3 cmH20/s for smog-group-2 vs. -3675±242.0 cmH20/s for FA; p<0.05). Time to ischemic contracture was also significantly prolonged in smog-group-1 (17.3±0.5 min) compared to FA (13.2±1.4 min; p