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). 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. 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. 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.

中文翻译：

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暴露于浓缩的环境颗粒物质可导致自发性高血压大鼠的心脏重量可逆地增加。

暴露于环境PM2.5会增加心血管疾病的死亡率和发病率。为了描述潜在的生物学机制，我们调查了慢性暴露于浓环境PM2.5（CAP）对心血管反应的时间依赖性。将自发性高血压大鼠（SHR）暴露于CAP 15周，并在不同时间点测量血压（BP），心脏功能和结构以及肺，下丘脑和心脏的炎症。长期暴露于CAP会显着增加BP，而从CAP暴露中退出可恢复BP。与它的BP效应相一致，长期暴露于CAP会显着降低SHR的心搏量和输出量，并伴有心脏重量增加和肥厚标志物ACTA1和MYH7的心脏表达增加。从CAP暴露中退出可恢复心脏功能，体重，以及肥厚标志物的表达，支持了心脏功能障碍和肥大继发于高血压的观念。与全身性炎症在介导CAP暴露对心血管的影响中的作用相一致，长期暴露于CAP显着增加了肺，心脏和下丘脑中促炎性细胞因子的表达。但是，退出暴露可以解决心脏和下丘脑的炎症，但不能解决肺部的炎症，这表明CAP暴露诱发的全身性炎症可能与肺部炎症无关。长期暴露于CAP会诱发可逆的心脏功能障碍和肥大，这很可能是在BP升高并诱发全身性炎症之后，这由多种组织中促炎性细胞因子的mRNA表达增加所证明。