After 2% of body weight fluid infusion, the homeostasis of fluid distribution was temporally modulated in spontaneously hypertensive rats, which is an animal model of neurodegenerative disease. After fluid infusion, shortened T2 showed in hippocampus and ventricles, and prolonged T2 was in corpus callosum and amygdala. The analysis of T2 distribution with rNNLS showed that a component with T2 around 100-200ms was increased in both T2-altered regions. We attributed this component as a restricted interstitial fluid, which could be correlated to the function of
Introduction
The fluid distribution in brain tissue is in a homeostasis state. However, the robustness of this homeostasis state may be weakened with neurodegenerative disease. The recently discovered glymphatic system demonstrated that the brain fluid circulation contributed to the waste clearance, and the dysfunction of fluid circulation could be associated with neurodegenerative disorders. Spontaneously hypertensive rat (SHR) is a good choice for this study, due to its propensity of dementia and AD.1,2 According to our previous study, water administration of 2% body weight at SHR induced T2 prolonging or shortening in some brain regions, while the control group of Wistar Kyoto rat had no apparent change.3 In this study, we investigate the tissue fluid distribution within voxels by analyzing the multiple spin echo sequence using regularized non-negative least square (rNNLS), which produces robust analyses of multi-component T2 decay curves in terms of a smooth T2 distribution.4Materials and Methods
SHR rats were anesthetized by 1.5 % isoflurane and injected with normal saline (2ml/100g) via tail vein at 7T Bruker Clinscan MRI scanner. Multi-echo spin echo images were acquired before and right after infusion, with the following parameters: TR = 3000ms, TE: from 10 to 320ms with an interval of 10ms, matrix size = 256x256, FOV = 35mm, slice number = 3, slice thickness = 1.5mm, distant factor = 10%. The pre- and post-injection T2 maps were calculated by a monoexponential fitting on all even echoes. T2 distribution was calculated by the even echoes as well with regularized non-negative least square (rNNLS) with 120 logarithmically spaced from 1ms to 2000ms. The regularizer μ is adjusted iteratively until χ2 in the interval between 1.02χ2min and 1.025χ2min, where the χ2min is the unregularized result. Four components of T2 are separated into myelin water (under 30ms, MW) fraction, intra/extracellular water (31-100ms, IEW) fraction, restricted interstitial fluid (100-200ms, rISF) fraction, and CSF (over 200ms) fraction.Results
T2 mapping of one representative SHR was shown in fig. 1. In all SHR (N=7), hyperintensity of T2 map was observed at enlarged ventricles and hippocampus (HC), and it can be attributed to the brain tissue atrophy.2 Significantly shortened T2 was observed in ventricles and HC regions, while significantly prolonged T2 was in corpus callosum (CC) and amygdala (AM). The ROIs were semi-automatically chosen on a T2W image in fig. 2. The rNNLS fitted T2 distribution of these ROIs were shown in fig.3 with log-scaled time axis. In T2-shortened regions (ventricles and HC), the value of MWF was decreased, CSF fraction was left-shifted to rISF fraction. Therefore, the overall T2 was shortened. In the T2-prolonged regions, the rISF and CSF contributed only 2% before infusion. After infusion, a significant increase in the rISF fraction appeared, and lead to the increase of overall T2. In grey matter, all component fraction was unchanged after infusion. For further spatial visualization, we demonstrated the fluid fraction maps of each component before and after infusion in fig. 4. The rISF showed a significant increase, and the regions are consistent with both T2-shortened and T2-prolonged regions in fig. 1. Furthermore, a clear increase also observed in the MW fraction.