Pulmonary Oxidative Stress, Inflammation, and Dysregulated Iron Homeostasis in Rat Models of Cardiovascular Disease

摘要: Underlying cardiovascular disease (CVD) is a risk factor for the exacerbation of air pollution health effects. Pulmonary oxidative stress, inflammation, and altered iron (Fe) homeostasis secondary to CVD may influence mammalian susceptibility pollutants. Rodent models are increasingly used examine mechanisms variation in susceptibility. Baseline cardiac pulmonary was characterized healthy normotensive Wistar Kyoto (WKY) rats, compromised spontaneously hypertensive rats (SHR), heart failure (SHHF) rats. Blood pressure, rate, breathing frequencies were measured 11 12 wk age, followed by necropsy at 14 15 age. pressure rate increased SHR SHHF relative WKY (SHR > WKY). Increased frequency WKY) resulted greater minute volume WKY. Bronchoalveolar lavage fluid (BALF) protein neutrophils higher (SHHF >> Lung ascorbate glutathione levels low BALF Fe-binding capacity decreased associated with transferrin (Trf) ferritin. However, lung ferritin lower Trf or mRNA markers inflammation stress (macrophage inflammatory [MIP]-2, interleukin [IL]-1alpha, heme oxygenase [HO]-1) rose but not whereas receptors 1 2 Four exhibited hypertrophy despite normal blood while demonstrating some complications noted earlier. This study demonstrates that display underlying such as impaired Fe than which play role rats' pollution.