Biological effects of diesel exhaust particles (DEP) on isolated cardiac muscle of guinea pigs

Res Commun Mol Pathol Pharmacol. 1994 Oct;86(1):99-110.

Abstract

Diesel engine-powered vehicles emit some 30 to 100 times more particles than do gasoline engine cars. We previously reported that diesel exhaust particles (DEP) could produce superoxide anions in an in vitro study. Furthermore, mice instilled intratracheally with DEP showed high mortality at low doses. The cause of death was lung edema with damage to the lung endothelial cells. In order to elucidate the mechanism of the onset of mortality induced by DEP, we examined the direct action of DEP on the isolated atrium of guinea pigs. A light-duty (2740cc), four cylinder diesel engine was used. The DEP were collected on fiberglass filter. DEP caused a negative inotropic action that was followed by the cardiac arrest of the isolated left atrium. These actions were not inhibited by propranolol, atropine, verapamil, diltiazem, diphenhydramine, indomethacin, superoxide dismutase or catalase. The precise mechanism of cardiac arrest is unknown. However, these results suggest that cardiac toxicity induced by DEP might be involved in lung edema.

MeSH terms

  • Animals
  • Cardiotonic Agents / pharmacology
  • Guinea Pigs
  • Heart / drug effects*
  • Heart Arrest / chemically induced
  • Heart Atria / drug effects
  • Heart Rate / drug effects
  • In Vitro Techniques
  • Male
  • Myocardial Contraction / drug effects
  • Particle Size
  • Vehicle Emissions / toxicity*

Substances

  • Cardiotonic Agents
  • Vehicle Emissions