Nanoparticle Inhalation Impairs Endothelium-Dependent Vasodilation in Subepicardial Arterioles

被引:87
作者
LeBlanc, A. J. [2 ]
Cumpston, J. L. [4 ]
Chen, B. T. [4 ]
Frazer, D. [2 ,4 ]
Castranova, V. [4 ]
Nurkiewicz, T. R. [1 ,2 ,3 ]
机构
[1] W Virginia Univ, Robert C Byrd Hlth Sci Ctr, Ctr Cardiovasc & Resp Sci, Morgantown, WV 26506 USA
[2] W Virginia Univ, Dept Physiol & Pharmacol, Morgantown, WV 26506 USA
[3] W Virginia Univ, Dept Neurobiol & Anat, Morgantown, WV 26506 USA
[4] NIOSH, Hlth Effects Lab Div, Pathol & Physiol Res Branch, Morgantown, WV USA
来源
JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES | 2009年 / 72卷 / 24期
基金
美国国家卫生研究院;
关键词
PARTICULATE AIR-POLLUTION; TITANIUM-DIOXIDE NANOPARTICLES; NITRIC-OXIDE; INTRATRACHEAL INSTILLATION; EPIDEMIOLOGIC EVIDENCE; MYOGENIC ACTIVITY; TERM EXPOSURE; MATTER; ULTRAFINE; MORTALITY;
D O I
10.1080/15287390903232467
中图分类号
X [环境科学、安全科学];
学科分类号
083001 [环境科学];
摘要
Exposure to fine particulate matter (PM, mean aerodynamic diameter <= 2.5 mu m) 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 TiO2 nanoparticles (primary particle diameter, similar to 21 nm) via inhalation at concentrations that produced measured depositions (10 mu g) relevant to ambient air pollution. Subepicardial arterioles(similar to 150 mm in diameter) were isolated and responses to transmural pressure, flow-induced dilation (FID), acetylcholine (ACh), the Ca2+ 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-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-induced 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.
引用
收藏
页码:1576 / 1584
页数:9
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