Mouse skeletal muscle creatine chemical exchange saturation transfer (CrCEST) imaging at 11.7T MRI

Mouse skeletal muscle creatine chemical exchange saturation transfer (CrCEST) imaging at 11.7T MRI
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DOI:
10.1002/jmri.26844
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发表时间:
2020-02-01
影响因子:
4.4
通讯作者:
Yoshioka, Yoshichika
Yoshioka, Yoshichika
中科院分区:
医学2区
文献类型:
--
作者:
Takahashi, Yusuke;Saito, Shigeyoshi;Yoshioka, Yoshichika

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背景肌酸化学交换饱和转移(CrCEST)显像有望成为评价肌肉能量代谢的新方法。目的建立小鼠骨骼肌CrCEST显像技术,并通过测定缺血后肢肌内Cr浓度的变化来验证该技术。研究类型前瞻性。动物模型C57 BL/6小鼠(n = 6)、轻度后肢缺血小鼠(n = 6)和重度后肢缺血小鼠(n = 6)。场强/序列磁共振血管造影(MRA)、CrCEST成像和磷磁共振波谱(P-31 MRS)在11.7 T下获得。评估MRA和P-31 MRS以确认橡胶止血带压迫后是否存在缺血。进行CrCEST成像,并在严重缺血模型、轻度缺血模型和对照小鼠中计算反映Cr浓度的磁化传递比不对称性(MTRasym)。在轻度缺血模型中,在缺血解除后进行随访CrCEST成像。统计检验平均值+/- SD,单因素方差分析(ANOVA)和Tukey HSD检验,非配对或配对t检验。结果MRA显示缺血后肢股动脉血流减少。P-31 MRS显示严重和轻度缺血后肢的PCr不同程度降低(每组n = 3,正常后肢:1.0 +/- 0,轻度缺血后肢:0.77 +/- 0.13,严重缺血后肢:0 +/- 0)。与对照组相比,CrCEST成像反向显示缺血后肢的MTRasym比率显著逐步增加(对照组、轻度缺血组和重度缺血组;分别为0.99 +/- 0.04、1.36 +/- 0.08和1.59 +/- 0.23,P < 0.0001)。此外,缺血缓解后的随访CrCEST成像显示MTRAsym比率正常化(恢复的后肢:1.01 +/- 0.05)。数据结论我们证明缺血后肢的MTRAsym增加,沿着PCr减少。我们证明了MTRasym在缺血释放后的正常化,并开发了小鼠骨骼肌的CrCEST成像。技术功效:第2阶段J. Magn. Reson。Imaging 2020;51:563-570.
Background Creatine chemical exchange saturation transfer (CrCEST) imaging is expected to be a novel evaluation method of muscular energy metabolism. Purpose To develop CrCEST imaging of mouse skeletal muscle and to validate this technique by measuring changes in Cr concentration of ischemic hindlimbs. Study Type Prospective. Animal Model C57BL/6 mice (n = 6), mild hindlimb ischemic mice (n = 6), and severe hindlimb ischemic mice (n = 6). Field Strength/Sequence Magnetic resonance angiography (MRA), CrCEST imaging, and phosphorus magnetic resonance spectroscopy (P-31 MRS) obtained at 11.7T. Assessment MRA and P-31 MRS were performed to confirm the presence of ischemia following the compression by rubber tourniquet. CrCEST imaging was performed and magnetization transfer ratio asymmetry (MTRasym), which reflects Cr concentration, and was calculated in severe ischemia models, mild ischemia models, and control mice. Follow-up CrCEST imaging was performed after the release of ischemia in the mild ischemia models. Statistical Tests Mean +/- SD, one-way analysis of variance (ANOVA) with Tukey's HSD test, unpaired or paired t-test. Results MRA revealed the loss of blood flow of the femoral artery in the ischemic hindlimb. P-31 MRS revealed different degrees of PCr decrease in severe and mild ischemic hindlimb (n = 3 per group, normal hindlimb: 1.0 +/- 0, mild ischemic hindlimb: 0.77 +/- 0.13, severe ischemic hindlimb: 0 +/- 0). CrCEST imaging inversely revealed a significant stepwise increase in the MTRasym ratio of ischemic hindlimbs compared with controls (control, mild ischemia, and severe ischemia; 0.99 +/- 0.04, 1.36 +/- 0.08, and 1.59 +/- 0.23, respectively, P < 0.0001). In addition, follow-up CrCEST imaging after the release of ischemia revealed normalization of the MTRasym ratios (recovered hindlimb: 1.01 +/- 0.05). Data Conclusion We demonstrated an increase in the MTRasym of ischemic hindlimbs, along with a decrease of PCr. We demonstrated the normalization of MTRasym after the release of ischemia and developed CrCEST imaging of mouse skeletal muscle. Technical Efficacy: Stage 2 J. Magn. Reson. Imaging 2020;51:563-570.