Department of Pharmacology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, 76 Yanta West Road, Xi'an, Shaanxi, 710061, China.
Department of Environmental Science and Engineering, Xi'an Jiaotong University, 28 Xianning West Road, Xi'an, Shaanxi, 710049, China.
Chemosphere. 2020 Dec;261:127710. doi: 10.1016/j.chemosphere.2020.127710. Epub 2020 Jul 16.
Existing experimental data do not sufficiently explain which pathophysiologic processes are involved in different age of rats exposed to long-term particulate matter. This study explored the pulmonary and cardiovascular effects of long-term PM and PM exposure in juvenile, adult and senescent rats. Tail cuff plethysmography, whole-body plethysmographic system, myograph, enzyme-linked immunosorbent assay, and inductively coupled plasma-mass spectrometry were used to detect the blood pressure, lung function, endothelium-dependent relaxation, inflammatory cytokines and heavy metals, respectively. The exposure time was from November, 2017 to October, 2018, and the average concentrations of PM and PM were 78.7 and 128.2 μg/m, respectively. Compared with the filtered air group, the body weight and survival rate in PM and PM exposure group were significantly decreased, and the survival rate of senescent exposed rats was only 30%. PM and PM exposure increased the blood pressure, elevated the levels of serum and bronchoalveolar lavage fluid inflammatory factors, and the senescent exposed rats showed an earlier rising trend in blood pressure and inflammatory factors than those of juvenile and adult exposed rats. Long-term PM and PM exposure could destroy intrapulmonary and small resistance arteries endothelial function, causing vasodilation disorders. PM and PM exposure caused particulate matter to accumulate in the lungs. Additionally, PM and PM exposure could also cause accumulation of cadmium (Cd) and lead in the liver, and chromium and Cd in the kidney. In conclusion, ambient PM and PM exposure induced particulate matter to accumulate in the body, caused severe pulmonary and vascular disorders, and demonstrated age-associated differences.
现有的实验数据还不能充分说明在不同年龄的大鼠中，哪些病理生理过程与长期暴露于颗粒物有关。本研究探讨了长期 PM 和 PM 暴露对幼年、成年和老年大鼠的肺和心血管的影响。尾套测压法、全身 plethysmography 系统、肌动描记器、酶联免疫吸附测定法和电感耦合等离子体质谱法分别用于检测血压、肺功能、内皮依赖性舒张、炎性细胞因子和重金属。暴露时间从 2017 年 11 月到 2018 年 10 月，PM 和 PM 的平均浓度分别为 78.7 和 128.2μg/m。与过滤空气组相比，PM 和 PM 暴露组的体重和存活率明显下降，老年暴露组的存活率仅为 30%。PM 和 PM 暴露增加了血压，升高了血清和支气管肺泡灌洗液中炎症因子的水平，老年暴露组的血压和炎症因子上升趋势早于幼年和成年暴露组。长期 PM 和 PM 暴露可破坏肺内和小阻力动脉内皮功能，引起血管舒张障碍。PM 和 PM 暴露使肺部颗粒物蓄积。此外，PM 和 PM 暴露还可导致肝脏中镉（Cd）和铅以及肾脏中铬和 Cd 的蓄积。总之，环境 PM 和 PM 暴露使颗粒物在体内蓄积，引起严重的肺和血管紊乱，并表现出与年龄相关的差异。
