PM2.5 exposure aggravates left heart failure induced pulmonary hypertension

• Published in: Acta Cardiologica 2019-05, Vol.74 (3), p.238-244
• Main Authors: Chen, Jun-Jiang, Ma, Wen-Ming, Yuan, Jing-Liang, Cui, Lian-Qun
• Format: Article
• Language: English
• Subjects: Air Pollutants - toxicity; Air Pollution - adverse effects; Animals; Arterial Pressure; Collagen Type III - metabolism; Disease Models, Animal; Disease Progression; Heart Failure - complications; Heart Failure - physiopathology; Hypertrophy, Right Ventricular - etiology; Hypertrophy, Right Ventricular - physiopathology; Inhalation Exposure; left heart failure; Lung - metabolism; Lung - pathology; lung fibrosis; Mice, Inbred C57BL; Particulate matter (PM2.5); Particulate Matter - toxicity; Pulmonary Arterial Hypertension - etiology; Pulmonary Arterial Hypertension - physiopathology; Pulmonary Artery - physiopathology; Pulmonary Fibrosis - etiology; Pulmonary Fibrosis - metabolism; Pulmonary Fibrosis - pathology; pulmonary hypertension; transforming growth factor beta; Transforming Growth Factor beta - metabolism; transverse aortic constriction; Ventricular Dysfunction, Left - complications; Ventricular Dysfunction, Left - physiopathology; Ventricular Function, Left
• ISSN: 0001-5385; 0373-7934; 1784-973X
• DOI: 10.1080/00015385.2018.1488568

Aim: Particulate matter 2.5 (PM2.5) exposure is high risk to cardiovascular diseases. We investigated the influence of PM2.5 exposure on pulmonary arterial hypertension (PAH) murine model induced by left ventricular (LV) failure. Methods: Thirty 10 weeks old C57BL/6 mice were randomised to four groups: sham group, sham + PM2.5 group, TAC group, and TAC + PM2.5 group. Eight weeks post TAC surgery, right ventricular (RV) and lung remodelling (Sirius Red staining and WGA Staining), heart and lung function (EF and RVSBP), and fibrotic genes (TGF-ti mRNA expression and collagen III protein level in lung tissue were measured. Results: Exposure to PM2.5 augments TAC induced PAH as evidenced by decreased EF value and increased RVSBP, RV cardiomyocytes size, RV and lung fibrosis, and upregulated expression of collagen III and TGF-a in comparison to TAC group in lung tissues. Even the LV EF value was deceased from 79.3 ± 3.4% to 63.4 ± 2.1% when sham group exposed to PM2.5, PM2.5 exposure had no effect on RVSBP, RV cardiomyocytes' size, RV weight/tibia length, RV and lung fibrosis, and expression of collagen III and TGF-a in sham surgery mice. Conclusions: Exposure to PM2.5 aggravates deterioration of LV failure induced PAH.