title: Elevation of serum endothelins and cardiotoxicity induced by particulate matter (PM2.5) in rats with acute myocardial infarction.
abstract: Epidemiological studies have defined a significant positive association of acute exposure to ambient concentrations of particulate matter (PM) with increased daily mortality and hospital admission for cardiovascular diseases. Experimental studies have shown that animals with pre-existing cardiovascular diseases are more susceptible to the cardiac effect of PM exposure. The present study was undertaken to investigate possible involvement of upregulation of the endothelin system in PM exposure-induced cardiotoxicity in rats with acute myocardial infarction (MI). Adult male Sprague Dawley rats were subjected to occlusion of the left coronary artery and displayed myocardial infarction 12 h after the surgery. The heart rate significantly decreased and premature ventricular complexes of the electrocardiogram occurred in the myocardial infarct animals. Exposure to PM(2.5) via intratracheal instillation with 2.0 mg in 0.3 mL normal saline significantly worsened the ventricular arrhythmia along with a further decrease in heart rate. The same PM exposure only caused slight cardiac changes in the sham-operated animals. Serum total endothelin concentrations were significantly elevated in both myocardial infarct rats and shamoperated controls in response to PM exposure. However, increased numbers of the endothelin receptor type A on the cardiomyocytes were observed only in the infarct myocardium. This study thus suggests that upregulation of the endothelin system in rats with MI is likely involved in the PM exposure-induced cardiotoxicity.
authors.affiliation: Department of Medicine, University of Louisville School of Medicine, KY 40292, USA. yjkang01@athena.louisville.edu
authors.forename: Y James
authors.initials: YJ
authors.lastname: Kang
authors.forename: Yan
authors.initials: Y
authors.lastname: Li
authors.forename: Zhanxiang
authors.initials: Z
authors.lastname: Zhou
authors.forename: Andrew M
authors.initials: AM
authors.lastname: Roberts
authors.forename: Lu
authors.initials: L
authors.lastname: Cai
authors.forename: Steven R
authors.initials: SR
authors.lastname: Myers
authors.forename: Lipeng
authors.initials: L
authors.lastname: Wang
authors.forename: Dale A
authors.initials: DA
authors.lastname: Schuchke
mesh_terms: D000280:Administration, Inhalation; D000393:Air Pollutants / Q000009:adverse effects* / Q000737:chemistry; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000139:chemically induced; D015415:Biomarkers / Q000097:blood; D023921:Coronary Stenosis / Q000097:blood; D004195:Disease Models, Animal; D004562:Electrocardiography; D016232:Endothelins / Q000097:blood* / Q000187:drug effects*; D006339:Heart Rate / Q000187:drug effects; D006352:Heart Ventricles / Q000187:drug effects / Q000378:metabolism; D007150:Immunohistochemistry; D008297:Male; D008955:Models, Cardiovascular; D009203:Myocardial Infarction / Q000097:blood*; D009206:Myocardium / Q000166:cytology / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism; D010316:Particle Size; D051381:Rats; D017207:Rats, Sprague-Dawley; D044022:Receptor, Endothelin A / Q000097:blood / Q000187:drug effects
chemical_list: D000393:Air Pollutants; D015415:Biomarkers; D016232:Endothelins; D044022:Receptor, Endothelin A