Suwa Tatsushi, Hogg James C, Quinlan Kevin B, Ohgami Akira, Vincent Renaud, van Eeden Stephan F
McDonald Research Laboratory and iCAPTURE Centre, University of British Columbia, St. Paul's Hospital, Vancouver, British Columbia, Canada.
J Am Coll Cardiol. 2002 Mar 20;39(6):935-42. doi: 10.1016/s0735-1097(02)01715-1.
We sought to determine the effect of exposure to air pollution particulate matter <10 microm (PM(10)) on the progression of atherosclerosis in rabbits.
Epidemiologic studies have associated exposure to ambient PM(10) with increased cardiovascular morbidity and mortality. We have previously shown that PM(10) exposure induces a systemic inflammatory response that includes marrow stimulation, and we hypothesized that this response accelerates atherosclerosis.
Watanabe heritable hyperlipidemic rabbits were exposed to PM(10) (n = 10) or vehicle (n = 6) for four weeks, and bone marrow stimulation was measured. Quantitative histologic methods were used to determine the morphologic features of the atherosclerotic lesions.
Exposure to PM(10) caused an increase in circulating polymorphonuclear leukocytes (PMN) band cell counts (day 15: 24.6 +/- 3.0 vs. 11.5 +/- 2.7 x 10(7)/l [PM(10) vs. vehicle], p < 0.01) and an increase in the size of the bone marrow mitotic pool of PMNs. Exposure to PM(10) also caused progression of atherosclerotic lesions toward a more advanced phenotype. The volume fraction (vol/vol) of the coronary atherosclerotic lesions was increased by PM(10) exposure (33.3 +/- 4.6% vs. 19.5 +/- 3.1% [PM(10) vs. vehicle], p < 0.05). The vol/vol of atherosclerotic lesions correlated with the number of alveolar macrophages that phagocytosed PM(10) (coronary arteries: r = 0.53, p < 0.05; aorta: r = 0.51, p < 0.05). Exposure to PM(10) also caused an increase in plaque cell turnover and extracellular lipid pools in coronary and aortic lesions, as well as in the total amount of lipids in aortic lesions.
Progression of atherosclerosis and increased vulnerability to plaque rupture may underlie the relationship between particulate air pollution and excess cardiovascular death.
我们试图确定暴露于空气污染细颗粒物（PM10，直径小于10微米）对兔动脉粥样硬化进展的影响。
流行病学研究表明，暴露于环境中的PM10与心血管疾病发病率和死亡率增加有关。我们之前已表明，暴露于PM10会引发包括骨髓刺激在内的全身炎症反应，我们推测这种反应会加速动脉粥样硬化。
将渡边遗传性高脂血症兔暴露于PM10（n = 10）或赋形剂（n = 6）中4周，并测量骨髓刺激情况。采用定量组织学方法确定动脉粥样硬化病变的形态学特征。
暴露于PM10导致循环中的多形核白细胞（PMN）杆状核细胞计数增加（第15天：24.6±3.0对11.5±2.7×10⁷/l [PM10对赋形剂]，p < 0.01），且PMN骨髓有丝分裂池大小增加。暴露于PM10还导致动脉粥样硬化病变向更晚期表型发展。PM10暴露使冠状动脉粥样硬化病变的体积分数（体积/体积）增加（33.3±4.6%对19.5±3.1% [PM10对赋形剂]，p < 0.05）。动脉粥样硬化病变的体积分数与吞噬PM10的肺泡巨噬细胞数量相关（冠状动脉：r = 0.53，p < 0.05；主动脉：r = 0.51，p < 0.05）。暴露于PM10还导致冠状动脉和主动脉病变中的斑块细胞更新及细胞外脂质池增加，以及主动脉病变中脂质总量增加。
动脉粥样硬化进展以及斑块破裂易感性增加可能是空气中颗粒物污染与心血管死亡过量之间关系的基础。
