Our news editors obtained a quote from the research, "To test this hypothesis in a normal animal model, rats were exposed to aerosols of carbon nanofibers (CNF) for 13 weeks. The highest CNF concentration (25 mg/m(3)) produced persistent respiratory tract (RT) inflammation/cytotoxicity throughout the exposure and 3-month recovery period, concomitant with translocation of inhaled CNF from airspace to extrapulmonary sites. The finding provided a basis for postulating that local RT effects could translocate to the systemic circulation, thereby producing CV alterations such as inflammation and/or coagulation changes. Therefore, assessments of cardiovascular endpoints such as cardiomyocyte cell proliferation (CP)/histopathology, C-reactive protein (CRP) levels, and 4 different diagnostic coagulation parameters, were investigated. No significant differences were measured between air or CNF-exposed rats when measuring fibrinogen levels, platelet counts, PT and aPTT bleeding times, and CRP levels. In addition, CP and histopathology evaluations were not different in CNF-exposed rats. Cardiac physiology and telemetry responses were not measured in this study."
According to the news editors, the research concluded: "It was concluded that no apparent cross-talk was evident between local respiratory and systemic/cardiovascular compartments."
For more information on this research see: Subchronic inhalation of carbon nanofibers: No apparent cross-talk between local pulmonary and cardiovascular/systemic responses. Carbon, 2013;62():165-176. Carbon can be contacted at:
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