Biexponential parameterization of diffusion and T2 relaxation decay curves in a rat muscle edema model:: Decay curve components and water compartments

Biexponential parameterization of diffusion and T2 relaxation decay curves in a rat muscle edema model:: Decay curve components and water compartments
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DOI:
10.1002/mrm.20610
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发表时间:
2005-09-01
影响因子:
3.3
通讯作者:
Mulkern, RV
Mulkern, RV
中科院分区:
医学3区
文献类型:
--
作者:
Ababneh, Z;Beloeil, H;Mulkern, RV

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定量的T-2松弛和扩散成像研究的大鼠肌肉水肿模型进行,以确定内和细胞外的水区室各自的衰减曲线的影响。用角叉菜胶溶液注射大鼠的右后爪以产生水肿肌肉。使用Carr-Purcell-Meiboom-Gill(CPMG)成像序列从两只爪获取T-2弛豫衰减曲线。然后使用线扫描扩散成像(LSDI)序列在宽b因子范围内从相同爪获取扩散衰减曲线。从水肿肌肉(EM)和对照肌肉(CM)两者进行测量。EM和CM的T-2弛豫衰减曲线与双指数函数拟合最好。快速T-2组分的分数从CM中的约0.95急剧下降到EM中的0.45,这与水区室模型一致,其中快速和慢速T-2组分分别反映细胞内和细胞外水。CM和EM扩散衰减曲线都需要双指数拟合函数,并且EM中快分量和慢分量的扩散系数比CM大得多。快速扩散成分的分数,但是,没有从根本上改变CM和EM条件(0.84与0.89 CM与EM)。假设一个模型,其中内部和细胞外的水室负责的快速和缓慢的T-2-衰减组件和缓慢和快速的扩散衰减组件,分别导致不支持实验的扩散组件的分数大小。我们的结论是,内部和细胞外的水区室是一个合理的解释两个T-2衰减组件在CM和EM,但其他因素,如限制扩散和/或替代形式的水区室,如表面与体积水,最有可能有深远的影响扩散衰减曲线的精确形状,一个完整的理解,这将需要大量的理论工作。
Quantitative T-2 relaxation and diffusion imaging studies of a rat muscle edema model were performed in order to determine the effects of intra- and extracellular water compartmentation on the respective decay curves. The right hind paw of rats was injected with a carrageenan solution to generate edematous muscle. A Carr-Purcell-Meiboom-Gill (CPMG) imaging sequence was used to acquire T-2 relaxation decay curves from both paws. A line scan diffusion imaging (LSDI) sequence was then used to acquire diffusion decay curves from the same paws over a wide b-factor range. Measurements were made from both edematous muscle (EM) and control muscle (CM). The EM and CM T-2 relaxation decay curves were best fit with biexponential functions. The fraction of the fast T-2 component dropped dramatically from approximately 0.95 in CM to 0.45 in EM, consistent with a water compartmentation model in which the fast and slow T-2 components reflect intra- and extracellular water, respectively. Both CM and EM diffusion decay curves required biexponential fitting functions, and the diffusion coefficients of the fast and slow components were substantially larger in EM than CM. The fraction of the fast diffusion component, however, was not radically altered between CM and EM conditions (0.84 versus 0.89 for CM versus EM). Assuming a model in which intra- and extracellular water compartments are responsible for the fast and slow T-2-decay components and for the slow and fast diffusion decay components, respectively, leads to fractional sizes of the diffusion components that are not supported by experiment. We conclude that intra- and extracellular water compartmentation is a reasonable interpretation for the two T-2-decay components in both CM and EM but that other factors, such as restricted diffusion and/or alternate forms of water compartmentation like surface versus volume water, most probably have profound influences on the precise shapes of the diffusion decay curves, a complete understanding of which will require significant theoretical work.