Dataset Information

Contribution of blood to nuclear Overhauser effect at -1.6 ppm.

ABSTRACT:

Purpose

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.

Methods

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 = 400 s/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 Lorentzian fitting of CEST Z-spectra was performed to quantify the NOE(-1.6) signal.

Results

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.

Conclusion

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.

SUBMITTER: Cui J

PROVIDER: S-EPMC8616842 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:An often-employed strategy to enhance signals in (31) P MRS is the generation of the nuclear Overhauser effect (NOE) by saturation of the water resonance. However, NOE allegedly increases the variability of the (31) P data, because variation is reported in NOE enhancements. This would negate the signal-to-noise (SNR) gain it generates. We hypothesized that the variation in NOE enhancement values is not caused by the variability in NOE itself, but is attributable to measurement uncertainties in the values used to calculate the enhancement. If true, the expected increase in SNR with NOE would improve the repeatability of (31) P MRS measurements. To verify this hypothesis, a repeatability study of native and NOE-enhanced (31) P MRSI was performed in the brains of seven healthy volunteers at 7?T. The repeatability coefficient (RC) and the coefficient of variation in repeated measurements (CoVrepeat ) were determined for each method, and the 95% limits of agreement (LoAs) between native and NOE-enhanced signals were calculated. The variation between the methods, defined by the LoA, is at least as great as that predicted by the RC of each method. The sources of variation in NOE enhancements were determined using variance component analysis. In the seven metabolites with a positive NOE enhancement (nine metabolite resonances assessed), CoVrepeat improved, on average, by 15%. The LoAs could be explained by the RCs of the individual methods for the majority of the metabolites, generally confirming our hypothesis. Variation in NOE enhancement was mainly attributable to the factor repeat, but between-voxel effects were also present for phosphoethanolamine and (glycero)phosphocholine. CoVrepeat and fitting error were strongly correlated and improved with positive NOE. Our findings generally indicate that NOE enhances the signal of metabolites, improving the repeatability of metabolite measurements. Additional variability as a result of NOE was minimal. These findings encourage the use of NOE-enhanced (31) P MRSI. Copyright © 2015 John Wiley & Sons, Ltd.