Detection of unstable atheroma plague by contrast ultrasound imaging

动脉粥样硬化斑块的活动性取决于持续炎症的严重程度。因此，我们将声学造影应用于炎症成像。在超声发射暂停10分钟后，我们通过诊断超声压力获得肾脏图像，允许注射MB后的白细胞吞噬微泡(MB)。通过从这幅图像中减去灌注图像，我们从滞留(吞噬)的MB中提取信号。缺血再灌注组在髓质和肾炎模型肾皮质均可见阳性信号，与各模型中白细胞的分布情况基本一致。我们将这种成像方法应用于低灌注性炎症组织的小鼠后肢缺血模型，该模型更好地模拟了动脉粥样硬化斑块。类似的设置提供了代表保留的甲基溴的不透明。因此，使用普通的声压，我们可以通过设计时间来成像炎症组织中残留的微泡。然而，组织学评估…更多的安全性表明，成像后24小时，白细胞浸润加重，这是可能导致斑块破裂的不良副作用。为了避免这种副作用，未来需要设计一种具有高灵敏度的低声压计。然而，由于白细胞释放血管内皮生长因子和粒细胞集落刺激因子(G-SF)已用于治疗性血管生成，导致白细胞渗入的副作用可能适用于治疗性血管生成。我们将这种方法应用于相同的模型，发现与预先给予300微克G-CSF(这是单一治疗的最小有效剂量)相结合，它显著地进一步促进了血管生成。因此，使用现有设备的声学造影炎症成像可以评估白细胞的渗透或炎症的活动性，这决定了各自的病理程度，但加重了炎症。然而，这种副作用适用于促进治疗性血管生成，值得在未来的研究中进行优化。较少

Activity of atheroma plaque depends on the severity of ongoing inflammation. Therefore, we applied contrast ultrasound to inflammation imaging. We obtained images of kidneys by diagnostic ultrasound pressure after suspension of ultrasound emission for 10 minutes allowing phagocytosis of microbubbles (MB) by leukocytes following MB injection. By subtracting perfusion image from this image, we extracted signals from retained (phagocytosed) MB. The signal distributed in the medulla in the ischemia reperfusion model and in the cortex in the glomerulonephritis model, which well agreed with the distribution of leukocytes in respective models. We applied this imaging method to mouse hindlimbs ischemia model of hypoperfused-inflamed tissue that better mimics atheroma plaque. The similar settings provided an opacification that represents retained MB. Thus, using ordinary acoustic pressure we can image retained microbubbles in the inflamed tissue by devising timing. However, histological assessm … More ent of its safety revealed that leukocyte infiltration was aggravated after 24 hours of imaging, which was unfavorable side effect potentially causing plaque rupture. In order to avoid this side effect a low-acoustic pressure apparatus with advanced sensitivity needs to be devised in the future. However, the side effect causing leukocyte infiltration could be applicable to therapeutic angiogenesis, because leukocytes release vascular endothelial growth factor and granulocyte colony stimulating factor (G-SF) has been used in therapeutic angiogenesis. We applied this method to the same model and found that it significantly further augmented angiogenesis in combination with pre-administration of 300 microgram G-CSF which was minimum effective dose at monotherapy. Thus, inflammation imaging by contrast ultrasound using current apparatus can evaluate leukocyte infiltration or activity of inflammation which determine the severity of respective pathology, but aggravated inflammation. However, this side effect was applicable to enhancement of therapeutic angiogenesis which would be worth while optimizing in the future study. Less