Contribution of blood to nuclear Overhauser effect at -1.6 ppm.
Contribution of blood to nuclear Overhauser effect at -1.6 ppm.
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DOI：
10.1002/mrm.28973
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发表时间：
2022-01
影响因子：
3.3
通讯作者：
Zu Z
中科院分区：
文献类型：
--
作者：
Cui J;Zhao Y;Wang F;Gochberg DF;Zu Z
先前有报道称，在大鼠和人脑中，在水中- 1.6 ppm左右存在一种传递性核超载增强（rNOE）饱和转移效应，称为NOE(- 1.6)，一些出版物表明，这可能与血液有关。在这里，我们通过体内和离体实验研究NOE（−1.6）是否来自血液。为了评估体内血液对NOE（−1.6）的贡献，通过两种方法抑制大鼠脑血管内信号：(1)信号采集，弥散加权为b = 400s/mm2；(2)血管内注射5 mg/kg单晶氧化铁纳米颗粒（MION）。同时制备离体血样。信号是通过化学交换饱和转移（CEST）脉冲序列获得的。对CEST z谱进行多池Lorentizan拟合，量化NOE（−1.6）信号。无论有无扩散加权测量，拟合的体内NOE（−1.6）信号没有显著变化，但注射MION后信号明显减弱。离体血液的NOE（−1.6）信号弱于体内组织。考虑到脑内血容量相对较小，体内弥散加权实验和离体实验均表明NOE（−1.6）并非主要来自血液。MION体内实验的机制尚不清楚。MION不仅抑制来自血管内空间的MR信号，而且改变了血管周围空间的易感性。这一结果表明，尽管NOE（−1.6）不是主要来自血液，但它可能依赖于脉管系统。
A relayed nuclear Overhauser enhancement (rNOE) saturation transfer effect at around −1.6 ppm from water, termed NOE(−1.6), was previously reported in rat and human brain, and some publications suggest that it may be related to blood. Here, we studied whether the NOE(−1.6) arises from blood through in vivo and ex vivo experiments. To evaluate the contribution from in vivo blood to NOE(−1.6), intravascular signals in rat brain were suppressed by two approaches: (1) signal acquisition with a diffusion-weighting of b = 400s/mm2; (2) intravascular injection of 5 mg/kg monocrystalline iron oxide nanoparticle (MION). Ex vivo blood sample was also prepared. The signals were acquired using a chemical exchange saturation transfer (CEST) pulse sequence. Multiple-pool Lorentizan fitting of CEST Z-spectra was performed to quantify the NOE(−1.6) signal. There are no significant variations in the fitted in vivo NOE(−1.6) signals when measured with or without diffusion-weighting, but significant signal decease does occur after injection of MION. The NOE(−1.6) signal from ex vivo blood is weaker than that from in vivo tissues. Considering the relatively small volume of blood in brain, the in vivo experiments with diffusion weighting and the ex vivo experiments both suggest that the NOE(−1.6) is not mainly from blood. The mechanism for the in vivo experiments with MION are less clear. MION not only suppresses MR signals from intravascular space, but changes the susceptibility in the perivascular space. This result suggests that although the NOE(−1.6) is not mainly from blood, it may be vasculature dependent.
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影响因子：
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