Cardiac and vasular changes in mice after exposure to ultrafine particulate matter
Cardiac and vasular changes in mice after exposure to ultrafine particulate matter
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DOI：
10.1080/08958370701493456
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发表时间：
2007-01-01
影响因子：
2.1
通讯作者：
Wingard, Christopher J.
中科院分区：
文献类型：
--
作者：
Cascio, Wayne E.;Cozzi, Emily;Wingard, Christopher J.
环境空气颗粒物(PM)浓度升高与心肌梗死、中风和心律失常的风险相关，而超细颗粒物(UFPM)可能对心血管系统尤其有害。最近的流行病学研究开始提供机械性的见解，但啮齿动物模型仍然是探索潜在机制的宝贵工具。这篇文章回顾了我们实验室的一系列研究，证明了小鼠模型将健康效应与生物学机制联系起来的前景。具体地说，描述了从北卡罗来纳州教堂山收集的暴露于气管内注入100微克UFPM的6至10周龄雄性ICR小鼠的数据。对缺血/再灌注、血管功能和止血的研究进行了描述。总而言之，UFPM暴露使心肌梗死范围加倍，伴随着缺血和再灌流发作，同时增加了缺血后氧化应激。UFPM改变全身血管张力的内皮依赖和非独立调节；增加血小板数量、血浆纤维蛋白原和可溶性P-选择素水平；并减少出血时间，这意味着增强的血栓形成潜力。综合这些发现，这种小鼠急性暴露UFPM的模型表明，UFPM诱导血栓前状态并降低血管舒缩反应性，从而提供了关于UFPM如何导致与血栓形成和缺血相关的血管事件的洞察，并增加了梗塞的范围。
Increased ambient air particulate matter (PM) concentrations are associated with risk for myocardial infarction, stroke, and arrhythmia, and ultrafine PM (UFPM) might be particularly toxic to the cardiovascular system. Recent epidemiological studies are beginning to offer mechanistic insights, yet the rodent model remains a valuable tool to explore potential mechanisms. This article reviews a series of studies from our laboratory demonstrating the promise of mouse models to link health effects to biological mechanisms. Specifically, data from 6- to 10-wk-old male ICR mice exposed to intratracheal instillation of 100 mu g of UFPM collected from the Chapel Hill, NC airshed are described. Studies of ischemia/reperfusion, vascular function, and hemostasis are described. In summary, UFPM exposure doubles the size of myocardial infarction attendant to an episode of ischemia and reperfusion while increasing postischemic oxidant stress. UFPM alters endothelial-dependent and -independent regulation of systemic vascular tone; increases platelet number, plasma fibrinogen, and soluble P-selectin levels; and reduces bleeding time, implying enhanced thrombogenic potential. Taking these findings together, this model of acute UFPM exposure in the mouse indicates that UFPM induces a prothrombotic state and decreases vasomotor responsiveness, thereby offering insight into how UFPM could contribute to vascular events associated with thrombosis and ischemia and increasing the extent of infarction.