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CARDIOVASCULAR RESPONSES TO ULTRAFINE CARBON PARTICLE EXPOSURES IN RATS
Citation:
Harder, V., B. Lentner, A. Ziesenis, E. Karg, L. Ruprecht, U P. Kodavanti, A. Stampfl, J. Heyder, AND H. Schulz. CARDIOVASCULAR RESPONSES TO ULTRAFINE CARBON PARTICLE EXPOSURES IN RATS. Presented at American Thoracic Society Meeting, Atlanta, GA, May 17-22, 2002.
Description:
TD-02-042 (U. KODAVANTI) GPRA # 10108
Cardiovascular Responses to Ultrafine Carbon Particle Exposures in Rats.
V. Harder1, B. Lentner1, A. Ziesenis1, E. Karg1, L. Ruprecht1, U. Kodavanti2, A. Stampfl3, J. Heyder1, H. Schulz1
GSF- Institute for Inhalation Biology1, Institute of Toxicology3, D-85758 Neuherberg/Munich, Germany and EPA- NHEERL2, NC 27711, USA
Rationale: This study focused on the detection of cardiovascular responses resulting from ultrafine carbon particle (EC30) inhalation in rats.
Methods: Arterial blood pressure (BP), electrocardiogram (ECG), core temperature and the activity of 5 male unrestrained WKY rats (255?337g, 12-15 weeks) were recorded by radio telemetry over a 5 day period (12 h light/dark). 24 hour particle exposures were performed during day #3 of measurement using spark discharging to generate EC30 (37 nm; 10-7cm-3; 180 g?m-3). Data analysis was focused on dark periods recordings.
Results: Rats were exposed to an estimated lung burden of 10 g?24 h-1 and 5.5?1012 particles?24 h-1. During particle exposure the mean heart rate (HR) was increased by 21.5 ? 7.7 bpm. Systolic and diastolic BP remained unaltered during particle inhalation, but showed a moderate augmentation of 5.3 ? 4.3 mm Hg and 6.0 ? 5.4 mm Hg, respectively, in the night following the exposure.
Conclusions: EC30 particle inhalation in young healthy rats leads to heart rate elevation and to a delayed moderate increase in arterial BPs. These responses suggest different underlying mediation pathways and support the hypothesis of cardiovascular effects mediated by ultrafine PM.
This abstract is funded by