Department of Pulmonary and Critical Care Medicine, Qingdao Municipal Hospital, School of Medicine, Qingdao University, Qingdao, 266071, China.
Qingdao Key Lab for Common Diseases, Qingdao Hospital, University of Rehabilitation and Health Sciences, Qingdao, 266071, China.
Respir Res. 2024 Sep 28;25(1):348. doi: 10.1186/s12931-024-02976-y.
As one of the most common traffic-related pollutants, diesel exhaust (DE) confers high risk for cardiovascular and respiratory diseases. However, its impact on pulmonary vessels is still unclear.
To explore the effects of DE exposure on pulmonary vascular remodeling, our study analyzed the number and volume of small pulmonary vessels in the diesel engine testers (the DET group) from Luoyang Diesel Engine Factory and the controls (the non-DET group) from the local water company, using spirometry and carbon content in airway macrophage (CCAM) in sputum. And then we constructed a rat model of chronic DE exposure, in which 12 rats were divided into the DE group (6 rats with 16-week DE exposure) and the control group (6 rats with 16-week clean air exposure). During right heart catheterization, right ventricular systolic pressure (RVSP) was assessed by manometry. Macrophage migration inhibitory factor (MIF) in lung tissues and bronchoalveolar lavage fluid (BALF) were measured by qRT-PCR and ELISA, respectively. Histopathological analysis for cardiovascular remodeling was also performed.
In DET cohort, the number and volume of small pulmonary vessels in CT were positively correlated with CCAM in sputum (P<0.05). Rat model revealed that chronic DE-exposed rats had elevated RVSP, along with increased wall thickness of pulmonary small vessels and right the ventricle. What's more, the MIF levels in BALF and lung tissues were higher in DE-exposed rats than the controls.
Apart from airway remodeling, DE also induces pulmonary vascular remodeling, which will lead to cardiopulmonary dysfunction.
作为最常见的交通相关污染物之一，柴油废气（DE）对心血管和呼吸道疾病具有较高的风险。然而，其对肺血管的影响尚不清楚。
为了探究 DE 暴露对肺血管重构的影响，我们分析了来自洛阳柴油机厂的柴油机测试员（DET 组）和当地自来水公司的对照组（非 DET 组）的小肺血管数量和体积，采用肺功能检查和痰中气道巨噬细胞内的碳含量（CCAM）进行分析。然后，我们构建了一个大鼠慢性 DE 暴露模型，其中 12 只大鼠分为 DE 组（6 只大鼠进行 16 周 DE 暴露）和对照组（6 只大鼠进行 16 周清洁空气暴露）。在右心导管检查过程中，通过压力计评估右心室收缩压（RVSP）。通过 qRT-PCR 和 ELISA 分别测量肺组织和支气管肺泡灌洗液（BALF）中的巨噬细胞移动抑制因子（MIF）。还进行了心血管重构的组织病理学分析。
在 DET 队列中，CT 中小肺血管的数量和体积与痰中的 CCAM 呈正相关（P<0.05）。大鼠模型显示，慢性 DE 暴露大鼠的 RVSP 升高，同时肺小血管和右心室的壁厚度增加。此外，BALF 和肺组织中的 MIF 水平在 DE 暴露组大鼠中高于对照组。
除了气道重塑，DE 还会引起肺血管重塑，从而导致心肺功能障碍。
