title: Exposure to concentrated ambient particulate matter induces reversible increase of heart weight in spontaneously hypertensive rats.
abstract: BACKGROUND
  Exposure to ambient PM2.5 increases cardiovascular mortality and morbidity. To delineate the underlying biological mechanism, we investigated the time dependence of cardiovascular response to chronic exposure to concentrated ambient PM2.5 (CAP).
  
  
  METHODS
  Spontaneously hypertensive rats (SHR) were exposed to CAP for 15 weeks, and blood pressure (BP), cardiac function and structure, and inflammations of lung, hypothalamus, and heart were measured at different time points.
  
  
  RESULTS
  Chronic exposure to CAP significantly increased BP, and withdrawal from CAP exposure restored BP. Consistent with its BP effect, chronic exposure to CAP significantly decreased cardiac stroke volume and output in SHR, accompanied by increased heart weight and increased cardiac expression of hypertrophic markers ACTA1 and MYH7. Withdrawal from CAP exposure restored cardiac function, weight, and expression of hypertrophic markers, supporting the notion that cardiac dysfunction and hypertrophy is subsequent to hypertension. In agreement with the role of systemic inflammation in mediating the cardiovascular effects of CAP exposure, chronic exposure to CAP markedly increased expression of pro-inflammatory cytokines in lung, heart, and hypothalamus. However, withdrawal from exposure resolves inflammation in the heart and hypothalamus, but not in the lung, suggesting that CAP exposure-induced systemic inflammation may be independent of pulmonary inflammation.
  
  
  CONCLUSIONS
  Chronic exposure to CAP induces reversible cardiac dysfunction and hypertrophy, which is likely to be subsequent to the elevation in BP and induction of systemic inflammation as evidenced by increased mRNA expression of pro-inflammatory cytokines in diverse tissues.
authors.affiliation: Department of Cardiology, East Hospital, Tongji University School of Medicine, Shanghai, 200120, People's Republic of China. zying@medicine.umaryland.edu.|Department of Medicine Cardiology Division, University of Maryland School of Medicine, 20 Penn Street, Baltimore, MD, 21201, USA. zying@medicine.umaryland.edu.
authors.forename: Zhekang
authors.initials: Z
authors.lastname: Ying
authors.affiliation: Division of Geriatric Medicine, Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, People's Republic of China. xiaoyunxietj@126.com.
authors.forename: Xiaoyun
authors.initials: X
authors.lastname: Xie
authors.affiliation: Division of Environmental Health Sciences, College of Public Health, The Ohio State University, Columbus, OH, USA. yuntao.bai@osumc.edu.
authors.forename: Yuntao
authors.initials: Y
authors.lastname: Bai
authors.affiliation: Department of Cardiology, East Hospital, Tongji University School of Medicine, Shanghai, 200120, People's Republic of China. chen_minjie@hotmail.com.|Department of Medicine Cardiology Division, University of Maryland School of Medicine, 20 Penn Street, Baltimore, MD, 21201, USA. chen_minjie@hotmail.com.
authors.forename: Minjie
authors.initials: M
authors.lastname: Chen
authors.affiliation: Department of Medicine Cardiology Division, University of Maryland School of Medicine, 20 Penn Street, Baltimore, MD, 21201, USA. xwang2@medicine.umaryland.edu.
authors.forename: Xiaoke
authors.initials: X
authors.lastname: Wang
authors.affiliation: Department of Medicine Cardiology Division, University of Maryland School of Medicine, 20 Penn Street, Baltimore, MD, 21201, USA. xzhang1@medicine.umaryland.edu.
authors.forename: Xuan
authors.initials: X
authors.lastname: Zhang
authors.affiliation: Department of Environmental Health Sciences, University of Michigan, Ann Arbor, MI, USA. tomoko@umich.edu.
authors.forename: Masako
authors.initials: M
authors.lastname: Morishita
authors.affiliation: Division of Environmental Health Sciences, College of Public Health, The Ohio State University, Columbus, OH, USA. qsun@cph.osu.edu.
authors.forename: Qinghua
authors.initials: Q
authors.lastname: Sun
authors.affiliation: Department of Medicine Cardiology Division, University of Maryland School of Medicine, 20 Penn Street, Baltimore, MD, 21201, USA. srajagopalan@medicine.umaryland.edu.
authors.forename: Sanjay
authors.initials: S
authors.lastname: Rajagopalan
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure; D004195:Disease Models, Animal; D006973:Hypertension / Q000139:chemically induced* / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D017379:Hypertrophy, Left Ventricular / Q000139:chemically induced* / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D018995:Myosin Heavy Chains / Q000378:metabolism; D052638:Particulate Matter / Q000633:toxicity*; D011014:Pneumonia / Q000139:chemically induced / Q000378:metabolism; D011918:Rats, Inbred SHR; D013318:Stroke Volume; D013997:Time Factors; D018487:Ventricular Dysfunction, Left / Q000139:chemically induced* / Q000235:genetics / Q000378:metabolism / Q000503:physiopathology; D016277:Ventricular Function, Left
chemical_list: D000199:Actins; D018836:Inflammation Mediators; C000594638:MYH7 protein, rat; D052638:Particulate Matter; D018995:Myosin Heavy Chains