The James Hogg Research Centre, Providence Heart and Lung Institute, St. Paul's Hospital, University of British Columbia , Vancouver, BC , Canada.
Inhal Toxicol. 2013 Nov;25(13):725-34. doi: 10.3109/08958378.2013.844749.
Numerous studies have found an association between transiently increased particulate matter air pollution and acute adverse cardiovascular health effects; however, the mechanisms underlying these effects are not clear. Translocation of ultra-fine ambient particulate matter has been proposed to play a key role in these acute side effects. This study was designed to determine the contribution of circulating (translocated) diesel exhaust particles (DEPs) to the systemic and vascular effects.
C57 mice (10-week) received intravenous DEPs via tail vein injection. Following 1-h post-injection, inflammatory cytokines (IL-1β, IL-6 and TNF-α), peripheral blood cell counts, band cell counts, aortic endothelial function and vascular constriction were assessed. Thoracic aortae were isolated, and endothelial function was examined by measuring acetylcholine (ACh) and sodium nitroprusside (SNP)-stimulated vascular relaxation using a wire myograph. In addition, phenylephrine (PE)-stimulated vasoconstriction was also measured. The amount of DEPs deposited and trapped in tissues (the spleen, liver, lungs and heart) were quantified.
Acute systemic DEP exposure caused a significant increase in TNF-α, peripheral neutrophil and band cell counts. ACh and SNP-induced relaxation were not affected by acute systemic DEP exposure, neither was PE-stimulated constriction. There was a significantly increased DEP deposition in the spleen as well as in the liver. No significantly increased DEPs were detected in the lung and heart.
Here we show that circulating DEPs induce a systemic response characterized by increased TNF-α, peripheral granulocytes, but does not impact endothelial function. Our study also suggests that circulating particles are rapidly removed from the circulation and predominantly sequestered in the spleen and liver.
许多研究发现，空气中颗粒物污染的短暂增加与急性不良心血管健康影响之间存在关联；然而，这些影响的机制尚不清楚。超细微粒物质的转移被认为在这些急性副作用中起关键作用。本研究旨在确定循环（转移）的柴油机排气颗粒（DEP）对全身和血管效应的贡献。
C57 小鼠（10 周龄）通过尾静脉注射接受静脉内 DEP。注射后 1 小时，评估炎症细胞因子（IL-1β、IL-6 和 TNF-α）、外周血白细胞计数、带细胞计数、主动脉内皮功能和血管收缩。分离胸主动脉，通过使用线描记法测量乙酰胆碱（ACh）和硝普钠（SNP）刺激的血管舒张来评估内皮功能。此外，还测量了苯肾上腺素（PE）刺激的血管收缩。定量测定 DEP 在组织（脾、肝、肺和心脏）中的沉积和截留量。
急性全身 DEP 暴露导致 TNF-α、外周中性粒细胞和带细胞计数显著增加。ACh 和 SNP 诱导的舒张不受急性全身 DEP 暴露的影响，PE 刺激的收缩也不受影响。脾和肝中 DEP 的沉积明显增加。在肺和心脏中未检测到明显增加的 DEP。
我们的研究表明，循环 DEP 诱导以 TNF-α 增加、外周粒细胞增加为特征的全身反应，但不影响内皮功能。我们的研究还表明，循环颗粒从循环中迅速清除，并主要蓄积在脾脏和肝脏中。
