Center for Cardiovascular and Respiratory Sciences, West Virginia University School of Medicine, Morgantown 26506-9105, West Virginia, USA.
J Toxicol Environ Health A. 2009;72(24):1576-84. doi: 10.1080/15287390903232467.
Exposure to fine particulate matter (PM, mean aerodynamic diameter <or=2.5 microm) has been shown to be a risk factor for cardiovascular disease mortality and may contribute to acute coronary events such as myocardial infarction (MI). There is sufficient reason to believe that smaller particles, such as nanoparticles, might be even more detrimental than larger sized particles due to their increased surface area and higher pulmonary deposition. Our laboratory showed that nanoparticle inhalation impairs endothelium-dependent arteriolar vasodilation in skeletal muscle. However, it is not known whether coronary microvascular endothelial function is affected in a similar manner. Rats were exposed to filtered air (control) or TiO(2) nanoparticles (primary particle diameter, approximately 21 nm) via inhalation at concentrations that produced measured depositions (10 microg) relevant to ambient air pollution. Subepicardial arterioles ( approximately 150 mum in diameter) were isolated and responses to transmural pressure, flow-induced dilation (FID), acetylcholine (ACh), the Ca(2+) ionophore A23187, and sodium nitroprusside (SNP) were assessed. Myogenic responsiveness was preserved between groups. In addition, there was no difference in the vasodilation to SNP, signifying that smooth muscle sensitivity to nitric oxide (NO) is unaffected by nano-TiO(2) exposure. However, inhalation of nano-TiO(2) produced an increase in spontaneous tone in coronary arterioles and also impaired endothelium-dependent FID. In addition, ACh-induced and A23187-induced vasodilation was also blunted in arterioles after inhalation of nano-TiO(2). Data showed that nanoparticle exposure significantly impairs endothelium-dependent vasodilation in subepicardial arterioles. Such disturbances in coronary microvascular function are consistent with the cardiac events associated with particle pollution exposure.
暴露于细颗粒物（PM，空气动力学直径<=2.5 微米）已被证明是心血管疾病死亡率的一个风险因素，并可能导致急性冠状动脉事件，如心肌梗死（MI）。有充分的理由相信，由于其表面积增加和更高的肺部沉积，较小的颗粒，如纳米颗粒，可能比更大尺寸的颗粒更具危害性。我们的实验室表明，纳米颗粒吸入会损害骨骼肌中内皮依赖性小动脉血管舒张。然而，目前尚不清楚冠状动脉微血管内皮功能是否以类似的方式受到影响。大鼠通过吸入暴露于过滤空气（对照）或 TiO2 纳米颗粒（初级粒径约为 21nm），吸入浓度产生测量的沉积（10μg）与环境空气污染有关。亚心外膜小动脉（直径约 150μm）被分离，并评估了跨壁压力、血流诱导扩张（FID）、乙酰胆碱（ACh）、钙离子载体 A23187 和硝普钠（SNP）的反应。各组之间的肌原性反应性保持不变。此外，SNP 引起的血管扩张没有差异，表明纳米 TiO2 暴露对平滑肌对一氧化氮（NO）的敏感性没有影响。然而，纳米 TiO2 的吸入会增加冠状动脉小动脉的自发性张力，并损害内皮依赖性 FID。此外，在吸入纳米 TiO2 后，ACh 诱导和 A23187 诱导的血管扩张也减弱。数据表明，纳米颗粒暴露显著损害了心外膜下小动脉的内皮依赖性血管舒张。这种冠状动脉微血管功能的紊乱与与颗粒污染暴露相关的心脏事件一致。
