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Exposure for ultrafine carbon particles at levels below detectable pulmonary inflammation affects cardiovascular performance in spontaneously hypertensive rats*
Citation:
Upadhyay, S., T. Stoeger, V. Harder, R. Thomas, M. SCHLADWEILER, M. Semmler-Behnke, S. Takenaka, E. Karg, P. Reitmier, M. Bader, A. Stampfl, U. P. KODAVANTI, AND H. Schulz. Exposure for ultrafine carbon particles at levels below detectable pulmonary inflammation affects cardiovascular performance in spontaneously hypertensive rats*. Particle and Fibre Toxicology. BioMed Central Ltd, London, Uk, 4(5):19, (2008).
Impact/Purpose:
Our study demonstrates unique pattern of effect on cardiac physiology as a result of pulmonary complications associated with microvascular thrombosis and oxidative stress following inhalation of ultrafine carbon particles. This publication provides important information of how ultrafine particles, as pollutants or nano materials, may induce diverse systemic response
Description:
Rationale: Exposure to particulate matter is a risk factor for cardiopulmonary disease but the related molecular mechanisms are poorly understood. Previously we studied cardiovascular responses in healthy WKY rats following inhalation exposure to ultrafine carbon particles (UfCPs). Therefore, in the present study we sought to investigate cardiopulmonary responses on spontaneously hypertensive rats (SHRs) following inhalation ofUfCPs (24hrs, 172~g'm-3), to assess whether compromised animals (SHR) exhibit a different response pattern compared
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to healthy rats (WKY). Methods: Radio-telemetric analysis was use to detect the cardiovascular response in SHRs. UfCPs-mediated inflammatory responses were assessed from broncho-alveolar-lavage fluid (BALF), lung and blood. Additionally, biomarkers of blood pressure (BP; renin-angiotensin system), oxidative stress (hemeoxygenase-l), blood coagulation factors (tissue factor, plasminogen activator inhibitor), and endothelial function (endothelin-l; endothelial receptors A and B) were measured from lung and cardiac tissue. Results: Increased BP and heart rate (HR) by about 5% with a lag of 1-3 days were detected in UfCPs exposed SHRs. Inflammatory markers of BALF, lung (pulmonary) and blood (systemic level) were not affected in these animals. However, hemeoxygenase-l, endothelin receptor A and B, tissue factor, and plasminogen activator inhibitor showed a significant induction (-2.5-fold; p
