Academic Journal
Exposure to ultrafine carbon particles at levels below detectable pulmonary inflammation affects cardiovascular performance in spontaneously hypertensive rats.
| العنوان: | Exposure to ultrafine carbon particles at levels below detectable pulmonary inflammation affects cardiovascular performance in spontaneously hypertensive rats. |
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| المؤلفون: | Upadhyay, S., Stöger, T., Harder, V., Thomas, R.F., Schladweiler, M.C., Semmler-Behnke, M., Takenaka, S., Karg, E.W., Reitmeir, P., Bader, M., Stampfl, A., Kodavanti, U.P., Schulz, S. |
| المصدر: | Part. Fibre Toxicol. 5:19 (2008) |
| بيانات النشر: | BioMed Central |
| سنة النشر: | 2008 |
| المجموعة: | PuSH - Publikationsserver des Helmholtz Zentrums München |
| الوصف: | Background: Exposure to particulate matter is a risk factor for cardiopulmonary disease but the underlying molecular mechanisms remain poorly understood. In the present study we sought to investigate the cardiopulmonary responses on spontaneously hypertensive rats (SHRs) following inhalation of UfCPs (24 h, 172 mug.m-3), to assess whether compromised animals (SHR) exhibit a different response pattern compared to the previously studied healthy rats (WKY). Methods: Cardiophysiological response in SHRs was analyzed using radiotelemetry. Blood pressure (BP) and its biomarkers plasma renin-angiotensin system were also assessed. Lung and cardiac mRNA expressions for markers of oxidative stress (hemeoxygenase-1), blood coagulation (tissue factor, plasminogen activator inhibitor-1), and endothelial function (endothelin-1, and endothelin receptors A and B) were analyzed following UfCPs exposure in SHRs. UfCPs-mediated inflammatory responses were assessed from broncho-alveolar-lavage fluid (BALF). 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) were not affected. However, mRNA expression of hemeoxygenase-1, endothelin-1, endothelin receptors A and B, tissue factor, and plasminogen activator inhibitor showed a significant induction (~2.5-fold; p < 0.05) with endothelin-1 being the maximally induced factor (6-fold; p < 0.05) on the third recovery day in the lungs of UfCPs exposed SHRs; while all of these factors - except hemeoxygenase-1 - were not affected in cardiac tissues. Strikingly, the UfCPs-mediated altered BP is paralleled by the induction of renin-angiotensin system in plasma. Conclusion: Our finding shows that UfCPs exposure at levels which does not induce detectable pulmonary neutrophilic inflammation, triggers distinct effects in the lung and also at the systemic level in compromised SHRs. These effects are characterized by increased activity of plasma renin-angiotensin ... |
| نوع الوثيقة: | article in journal/newspaper |
| وصف الملف: | application/pdf |
| اللغة: | English |
| تدمد: | 1743-8977 |
| Relation: | info:eu-repo/semantics/altIdentifier/pmid/ 19055790; info:eu-repo/semantics/altIdentifier/wos/000267423900001; info:eu-repo/semantics/altIdentifier/isbn/1743-8977; info:eu-repo/semantics/alt; https://push-zb.helmholtz-muenchen.de/frontdoor.php?source_opus=2213; urn:isbn:1743-8977; urn:issn:1743-8977 |
| DOI: | 10.1186/1743-8977-5-19 |
| الاتاحة: | https://push-zb.helmholtz-muenchen.de/frontdoor.php?source_opus=2213 https://doi.org/10.1186/1743-8977-5-19 |
| Rights: | info:eu-repo/semantics/openAccess |
| رقم الانضمام: | edsbas.5F8F5A57 |
| قاعدة البيانات: | BASE |
Full Text Finder | تدمد: | 17438977 |
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| DOI: | 10.1186/1743-8977-5-19 |