Nanoparticle inhalation impairs endothelium-dependent vasodilation in subepicardial arterioles.
Nanoparticle inhalation impairs endothelium-dependent vasodilation in subepicardial arterioles.
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DOI：
10.1080/15287390903232467
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发表时间：
2009
期刊：
影响因子：
--
通讯作者：
Nurkiewicz TR
中科院分区：
文献类型：
--
作者：
LeBlanc AJ;Cumpston JL;Chen BT;Frazer D;Castranova V;Nurkiewicz TR
暴露于细颗粒物（PM，平均空气动力学直径≤2.5 μm）已被证明是心血管疾病死亡的一个危险因素，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，较小的颗粒，如纳米颗粒，可能比较大的颗粒更有害，因为它们的表面积增加，肺部沉积更多。我们的实验室表明，吸入纳米颗粒会损害骨骼肌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。将大鼠吸入过滤后的空气（对照）或TiO2纳米颗粒（主要颗粒直径~21 nm），其浓度与环境空气污染相关（10 μg）。分离心外膜下小动脉（直径约150 μm），评估其对跨壁压力、血流诱导扩张（FID）、乙酰胆碱、Ca2+离子离子A23187和硝普钠（SNP）的反应。各组间肌原性反应保持不变。此外，对SNP的血管舒张没有差异，这表明平滑肌对一氧化氮（no）的敏感性不受纳米tio2暴露的影响。然而，吸入纳米tio2会增加冠状动脉的自发张力，也会损害内皮依赖性FID。此外，吸入纳米tio2后，ACh-和a23187诱导的血管舒张也在小动脉中减弱。数据显示，纳米颗粒暴露显著损害心外膜下小动脉内皮依赖性血管舒张。冠状动脉微血管功能紊乱与颗粒污染暴露相关的心脏事件一致。
Exposure to fine particulate matter (PM, mean aerodynamic diameter ≤ 2.5 μm) 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 lab showed that nanoparticle inhalation impairs endothelium-dependent arteriolar vasodilation in skeletal muscle. However, it is not known if coronary microvascular endothelial function is affected in a similar manner. Rats were exposed to filtered air (control) or TiO2 nanoparticles (primary particle diameter, ~21 nm) via inhalation at concentrations that produced measured depositions (10 μg) relevant to ambient air pollution. Subepicardial arterioles (~150 μm in diameter) were isolated and responses to transmural pressure, flow-induced dilation (FID), acetylcholine, the Ca2+ ionophore A23187, and sodium nitroprusside (SNP) 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-TiO2 exposure. However, inhalation of nano-TiO2 produced an increase in spontaneous tone in coronary arterioles and also impaired endothelium-dependent FID. In addition, ACh- and A23187-induced vasodilation was also blunted in arterioles after inhalation of nano-TiO2. 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.
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