Abstract
Although it is possible for inhalation of ultrafine particles to impair human health, its effect is not clear in patients with HFpEF. This study investigated cardiac and hemodynamic changes in hypertension-induced rats of HFpEF after inhaling ultrafine zinc particles for a while. Multiple experimental measurements were carried out in DSS rats fed with high salt (HS) and low salt (LS) diets as well as HS diet with the inhalation of ultrafine zinc particles (defined as HP). Cardiac strain and strain rate were quantified by the speckle tracking echocardiography. The pressure and flow waves were recorded in the carotid artery and abdominal aorta and analyzed by the models of Windkessel and Womersley types. HS and HP rats were found to show lower strains on endocardium and epicardium than LS rats. The inhalation of ultrafine zinc particles further reduced the strain in the longitudinal direction on the endocardium of rats with HFpEF, but had relatively small effects on the epicardium. The inhalation of ultrafine zinc particles resulted in the increase of systemic resistance and the decrease of total vascular compliance as well as the increased PWV and induced more severe vascular stiffening in rats with HFpEF. In summary, the inhalation of ultrafine zinc particles deteriorated local myocardial dysfunctions in the LV and the hemodynamic environment in peripheral arteries in rats of HFpEF. This study is of importance to understand the mechanisms of cardiovascular impairments owing to air pollution.
Highlights
Air quality has recently become a major concern in China
Protocol was consisted of three groups: LS group, HS group, and HP group, where 6 LS animals were fed with low salt diet, i.e., 0.3% sterile NaCl (Beijing KeaoXieli Feed Co., Ltd.) until they were at the age of 14 weeks; 8 HS animals were fed with high salt diet, i.e., 8% sterile NaCl until 14 weeks; and 8 HP animals were fed with high salt diet until 14 weeks, but started to inhale ultrafine zinc particles (∼50 nm, Beijing Deke Daojin Science And Technology Co., Ltd.) with the concentration of about 500 μg/m3 (Beckett et al, 2005; Wallenborn et al, 2008) when they were 10-week-old
Echocardiographic measurements show that HS and HP groups have a significant decrease of cardiac output (CO) (78.98 ± 3.48 in LS vs. 58.36 ± 2.39 in HS vs. 47.84 ± 4.28 in HP) and E/A ratio (1.41 ± 0.07 in LS vs. 0.96 ± 0.05 in HS vs. 0.92 ± 0.06 in HP) as compared with the LS group
Summary
The exposure to particulate matter air pollution, in PM0.1 (ultrafine particles), significantly deteriorates cardiovascular diseases and heart diseases (Mills et al, 2009; Shah et al, 2013; Hwang et al, 2014; Brook et al, 2018). E.g., ultrafine zinc particles, leads to vascular dysfunctions by increasing endothelial oxidative stress (Mills et al, 2005; Wauters et al, 2013) such that it may accelerate the development of HFpEF. As a logic starting point, HS-feeding DSS rats were made inhaling ultrafine zinc particles to find the hemodynamic mechanisms for potential deterioration of HFpEF due to air pollution
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