Systemic injection of planktonic forms of mammalian-derived nanoparticles alters arterial response to injury in rabbits.

Systemic injection of planktonic forms of mammalian-derived nanoparticles alters arterial response to injury in rabbits.
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全身注射浮游形式的哺乳动物衍生纳米颗粒会改变兔子对损伤的动脉反应。

DOI:
10.1152/ajpheart.00993.2008
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发表时间:
2009
期刊:
American journal of physiology. Heart and circulatory physiology
影响因子:
--
通讯作者:
Miller,VirginiaM
Miller,VirginiaM
中科院分区:
--
文献类型:
--
作者:
Schwartz,MariaK;Lieske,JohnC;Hunter,LarryW;Miller,VirginiaM

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设计实验以检验以下假设:源自钙化的患病人体组织或牛血的纳米颗粒(NP)的渗透形式的全身递送是加剧动脉对损伤的反应的可传播颗粒。将生理盐水(对照)、脂多糖(LPS;亚临床感染的替代物)、羟基磷灰石晶体(HA; NP壳的替代物)、暴露于培养基的HA晶体或牛或人来源的NP的渗透形式静脉内注射到从一个颈动脉机械去除内皮的新西兰白色兔中。超声监测颈动脉5 wk后取颈动脉行组织学检查。各组所有动物的未受伤动脉保持通畅,解剖结构正常。注射人源NP的11只动物中有6只动物的损伤动脉闭塞和/或钙化;其他组动物的损伤动脉均未闭塞(n= 28;P≤ 0.05)。注射内毒素或透明质酸晶体的兔损伤动脉出现偏心性增生。不连续的内部弹性层和变薄的媒体特征动脉从动物注射牛源性纳米粒子或培养的HA晶体。总之,与牛源性NP和其他炎性试剂不同,全身施用促炎性形式的人源性NP加剧了动脉对损伤的反应。
Experiments were designed to test the hypothesis that the systemic delivery of planktonic forms of nanoparticles (NPs) derived from calcified, diseased human tissue or bovine blood are transmissible particles that exacerbate arterial response to injury. New Zealand White rabbits in which the endothelium was mechanically removed from one carotid artery were injected intravenously with either saline (control), lipopolysaccharide (LPS; surrogate for subclinical infection), hydroxyapatite crystals (HA; surrogate for NP shell), HA crystals exposed to culture media, or planktonic forms of bovine- or human-derived NPs. Carotid arteries were monitored by ultrasonography for 5 wk and then removed for histological examination. Uninjured arteries from all animals in each group remained patent with a normal anatomy. Injured arteries from 6 of 11 animals injected with human-derived NPs occluded and/or calcified; none of the injured arteries from animals in the other groups occluded (n= 28;P≤ 0.05). Injured arteries of rabbits injected with LPS or HA crystals developed eccentric hyperplasia. Discontinuous internal elastic laminae and thinning media characterized arteries from animals injected with bovine-derived NPs or cultured HA crystals. In conclusion, the systemic administration of planktonic forms of human-derived NPs exacerbated arterial response to injury distinct from that of bovine-derived NPs and other inflammatory agents.
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