title: Ambient particulate matter affects cardiac recovery in a Langendorff ischemia model.
abstract: Exposure to ambient particulate matter (PM) is associated with increased mortality and morbidity among subjects with cardiovascular impairment. We hypothesized that exposure of spontaneously hypertensive (SH) rats to PM impairs the recovery of cardiovascular performance after coronary occlusion and reperfusion-ischemia. SH rats were exposed by intratracheal instillation to saline, standard urban PM (Ottawa dust EHC-93, 10 mg/kg body weight) or endotoxin (lipopolysaccharides LPS, 350 EU/animal) to induce a similar pulmonary inflammation. At 4 h postexposure, hearts were isolated and retrograde perfused in a Langendorff model. The experimental protocol included 35 min of coronary occlusion followed by 120 min of reperfusion, during which left ventricular developing pressure (LDVP), coronary flow (CF), and heart rate (HR) were measured. Baseline LVDP in particle-instilled SH rats was significantly decreased compared to saline-instilled animals. In addition, after ischemia the recovery of LDVP was much slower in rats pretreated with PM or LPS compared to saline instilled rats. The direct effects of the soluble PM fraction and the role of Zn2+ were also tested cardiomyocytes (H9C2 cells). Both particle-free filtrate and Zn2+ inhibited ATP or ionophore-stimulated calcium influx in cardiomyocytes. This inhibitory effect was related to an effect on calcium channels, as shown with Nifedipine. This study provides evidence that exposure to instillation of PM has reversible acute effects on the recovery of cardiac physiological parameters after ischemia. The effect may be caused by a direct action of soluble metals on calcium homeostasis in heart, but pulmonary inflammation may also play a significant role.
authors.affiliation: Particle Research, Institut fur Umweltmedizinische Forschung (IUF gGmhH) at the University of Düsseldorf, NRW, Germany.
authors.forename: Karim
authors.initials: K
authors.lastname: Bagate
authors.forename: James J
authors.initials: JJ
authors.lastname: Meiring
authors.forename: Miriam E
authors.initials: ME
authors.lastname: Gerlofs-Nijland
authors.forename: Flemming R
authors.initials: FR
authors.lastname: Cassee
authors.forename: Herbert
authors.initials: H
authors.lastname: Wiegand
authors.forename: Alvaro
authors.initials: A
authors.lastname: Osornio-Vargas
authors.forename: Paul J A
authors.initials: PJ
authors.lastname: Borm
mesh_terms: D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism; D003326:Coronary Circulation / Q000187:drug effects; D004195:Disease Models, Animal; D004359:Drug Therapy, Combination; D006352:Heart Ventricles / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects*; D006973:Hypertension / Q000473:pathology / Q000503:physiopathology; D066298:In Vitro Techniques; D007442:Intubation, Intratracheal; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D009543:Nifedipine / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D015427:Reperfusion Injury / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000503:physiopathology; D020257:Ventricular Remodeling / Q000187:drug effects*; D015032:Zinc / Q000494:pharmacology
chemical_list: D000393:Air Pollutants; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D008070:Lipopolysaccharides; D009543:Nifedipine; D015032:Zinc; D002118:Calcium