Quantification Of Brain Metabolite Concentrations In Acute Hypoxia Ischemic Brain Injury

The pathologic mechanism and energy metabolism of acute hypoxia ischemic braininjury have been explored for a long period. Magnetic Resonance Spectroscopy (MRS)can non-invasively provide biochemical information from distinct regions of brainthrough brain metabolic quantitation, which can be applied for hypoxia ischemicbrain injury detection, progressional monitoring and treatment.This study was divided two parts:Part 1: Objective: Our study are mainly focused on the influencing factors ofquantification analysis. LCModel and MRUI software have been employed to analyzesimulated spectra, which similar to those typically obtained at different echo-time(TE)/repetition time (TR) in the swine brain at 1 .ST. Method: Acute hypoxic ischemiapiglet model and an extemal standard phantom containing a detectable compounds ofknown concentration were studied by using 1. ST GE Signa scanner with a standardhead coil; the single-voxel proton magnetic resonance spectroscopy (1H-MRS) datawas acquired from the 20-mm cubic VOI, which were placed in both the swine brainand external standard solution. The PRESS sequence was used with TE=26/135msec, TR=1500/2500msec, and 128 scan averages were performed. Thequantification of N-acetylaspartate(NAA), creatine(Cr) were accomplished by theLCModel and QUEST algorithm of MRUI. Results: In the LCModel group, the meanconcentration of NAA was 10.34±4.60 mmol/kg, while Cr was 6.52±1.86mmol/kg. In the QUEST group, the mean concentration of NAA was 10.16±0.93mmol/kg, and Cr was 5.47±1.5mmol/kg. There were no statistically significantdifferences between the LCModel and QUEST group of NAA concentration(P＞0.05).However, both the concentration of Cr in LCModel and QUEST group weresignificantly reduced while compared to the Cr values in normal group. Conclusion:Different TE/TR values have greatly influence on quantification analysis.Part 2: Objective: To explore the dynamic changes of brain metabolite in acutehypoxia ischemia brain injury rat model. Method: 104 rats were divided into 13groups randomly. Each group had 8 rats and all rats were sacrificed by cutting head. Concerning the time course, the rat head was dropped into liquid nitrogen at timepoints: 0 sec, 20 sec, 40 sec, 60 sec, 2 min, 3 min, 4 min, 6 min, 8 min, 10 min, 12min, 14 min, 16 min, 18 min, and 2 0 min. The N-acetylaspartate, lactate and creatineconcentration in rat brain were measured by high performance liquid chromatographymethod. Results: While the ischemia time delayed from 0 sec to 20 sec, brain lactateconcentration increased rapidly while NAA and Cr concentrations decreased. After 4min the lactate concentration keep on increasing. The concentration of NAA wastemporarily increased between 3min-14min. Conclusion: lactate, NAA and Crconcentrations were dynamically changed with ischemic time in acute hypoxiaischemic brain injury.