Cardiovascular and lung inflammatory effects induced by systemically administered diesel exhaust particles in rats

Am J Physiol Lung Cell Mol Physiol. 2007 Mar;292(3):L664-70. doi: 10.1152/ajplung.00240.2006. Epub 2006 Nov 3.

Abstract

Pollution by particulates has consistently been associated with increased cardiorespiratory morbidity and mortality. It has been suggested that ultrafine particles, of which diesel exhaust particles (DEP) are significant contributors, are able to translocate from the airways into the bloodstream in vivo. In the present study, we assessed the effect of systemic administration of DEP on cardiovascular and respiratory parameters. DEP were administered into the tail vein of rats, and heart rate, blood pressure, blood platelet activation, and lung inflammation were studied 24 h later. Doses of 0.02, 0.1, or 0.5 mg DEP/kg (8, 42, or 212 microg DEP/rat) induced a significant decrease of heart rate and blood pressure compared with saline-treated rats. Although the number of platelets was not affected, all the doses of DEP caused a shortening of the bleeding time. Similarly, in addition to triggering lung edema, the bronchoalveolar lavage analysis revealed the presence of neutrophil influx in DEP-treated rats in a dose-dependent manner. We conclude that the presence of DEP in the systemic circulation leads not only to cardiovascular and haemostatic changes but it also triggers pulmonary inflammation.

MeSH terms

  • Animals
  • Bleeding Time
  • Blood Pressure / drug effects
  • Cardiovascular Diseases / chemically induced*
  • Cardiovascular Diseases / pathology
  • Erythrocyte Count
  • Heart / drug effects*
  • Heart Rate / drug effects
  • Leukocyte Count
  • Lung / drug effects*
  • Male
  • Pneumonia / chemically induced*
  • Pneumonia / pathology
  • Pulmonary Edema / chemically induced
  • Pulmonary Edema / pathology
  • Rats
  • Rats, Inbred WKY
  • Vehicle Emissions / toxicity*

Substances

  • Vehicle Emissions