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ULTRAFINE PARTICULATE MATTER EXPOSURE ATTENUATES MOUSE AORTIC RELAXATIONS
Citation:
WINGARD, C. J., E. COZZI, B. TUTTLE, R. M. LUST, R. VAN SCOTT, W. CASCIO, AND R. B. DEVLIN. ULTRAFINE PARTICULATE MATTER EXPOSURE ATTENUATES MOUSE AORTIC RELAXATIONS. Presented at Federation of American Societies for Experimental Biology Annual Meeting, San Francisco, CA, April 01 - 05, 2006.
Description:
Particulate air pollution (PM) contributes to adverse cardiovascular events by yet unknown mechanisms. We tested the hypothesis that PM exposure altered endothelial regulation of systemic vascular tone. 6-10 week old male ICR mice were exposed to a single dose of 10, 30 or 100 'g of ultrafine PM or vehicle by intratracheal instillation. 24 hours later aortas were isolated and exposed to phenylephrine (PE), acetylcholine (ACH) or adenosine to probe their vascular responses. Constrictor responses to PE were not different between PM exposed and control aortas. PM exposure attenuated ACH relaxation in a dose-dependent manner.
Control PM-exposed
10 p~ %ACH
Relaxation 64.6 ? 1 1.8 68.5 , 7.0
EC;tr(AM) 12?0.6 0.3+0.1*
30 pg %ACH
Relaxation 62.8 , 8.5 1.1 , 0.7
ECs(' (?M) 77.8 , 6.5 * 0.4 , 0.1 .
100 jig %ACH
Relaxation 49.5 + 6.5 63.3 , 10.1 *
EC;o(FM) 1.4, 0.9 0.5-1.0.1':
(*statistical significance from control , P< 0.05, n = 4-8)
In endothelial-denuded aortas PM exposure increased the maximal contractile response (mN mm2) to 10 'M adenosine (control 1.39 , 0.02 vs. PM-exposed 1.79 , 0.11*). These results indicate that PM exposure altered endothelial-dependent and independent vascular responsiveness and may contribute to cardiovascular complications. This abstract dose not necessarily represents EPA policy. Supported by Phillip Morris Foundation # 567881.