Article Figures & Data
Figures
- Fig 1.
Changes in 1H-MR spectroscopy spectra and lactate content in the BG within 72 hours after HI. 1H-MR spectroscopy spectra of the right BG of the control and HI model groups at 0–2, 2–6, and 6–12 hours are shown as A–D (lactate peak is located at 1.33 ppm). The lactate peak in the control group is low and flat (A) and peaked at 2–6 hours after HI (C). ROI selection (E): right BG (yellow solid red). The change in lactate content after HI is shown in F (we calibrated the results, assuming 80% brain-water content, 100% visibility of water signal, and 55.5 mol/L). The asterisk represents a statistical difference compared with the 2- to 6-hour time point. HIBI indicates hypoxic-ischemic brain injury.
- Fig 2.
[18F] FDG PET/CT images in the control group (A) and the time points of 6–12, 12–24, and 48–72 hours in the HI model groups (B–D). Changes in the SUVmax of the basal ganglia and BG/OC ratio of the BG in the control and HI model groups (E–F). The BG and OC of the control group (A) are clearly visible on [18F] FDG PET/CT images. [18F] FDG uptake was symmetrically distributed. At 6–12 hours after HI, the BG/OC ratio of the HI groups was greater than that of the control group (B). At 12–24 hours after HI, the BG/OC ratio in the BG was decreased compared with 6–12 hours (C). The BG/OC ratio was further decreased after 48–72 hours, and the BG and cortex showed less clearance (D). The SUVmax of the basal ganglia and BG/OC ratio peaked at 6–12 hours after HI. The hashtag represents a statistical difference compared with the 6- to 12-hour time points (E–F). Changes in lactate levels and the BG/OC ratio after HI (G). The left vertical axis represents the lactate content, and the right vertical axis represents the BG/OC ratio (G, the circle represents the average value of lactate content; the diamond represents the average value of BG/OC). Spearman correlation analysis showed that the lactate content was positively correlated with the BG/OC ratio (r = 0.74, P < .001; H). HIBI indicates hypoxic-ischemic brain injury.
- Fig 3.
H&E staining of the BG in the control and HI model groups. A–E, H&E-stained images of the control group and the 6-, 24-, 48-, and 72-hour time points of the HI model groups. Compared with the control group (A), we observed the following apparent pathologic changes: swelling in some astrocytes (B), many astrocytes and some neurons apparently swollen with visible vacuoles and karyopyknosis (C), and astrocytes apparently swollen and necrotic. Neurons also showed swelling and necrosis (D), the neuronal membranes were damaged, and nuclei were swollen and weakly stained. These observations were made at ×400 magnification (E).
- Fig 4.
Expression levels of MCT-2 and MCT-4 in the BG in the control and HI model groups (A–H) and change in expression levels of MCT-2 and MCT-4 in the BG after HI (I) and correlation with lactate content (J and K). A–D, MCT-2 expression in the control group and at 6, 24, and 48 hours after HI in the HI model groups. MCT-2 was mainly stained brown in the membrane of the neurons (A). Compared with the control group (A), MCT-2 staining at 6 and 24 hours after HI (B and C) was darker and greater numbers of positive cells were observed. MCT-2 expression was reduced at 48 hours (D). E–H, MCT-4 expression in the BG of the control group and at 6, 24, and 48 hours after HI in the model groups. MCT-4 was mainly expressed in the membranes of astrocytes (E). MCT-4 staining was darker at 6 and 24 hours after HI (F and G), compared with the control group (E). MCT-4 expression was reduced at 48 hours after HI (H). The expression levels of MCT-2 and MCT-4 were highest at 12–24 hours (I). Expression levels of MCT-2 and MCT-4 were positively correlated with the lactate level (J and K): MCT-2 (r = 0.47), MCT-4 (r = 0.38).
- Fig 5.
Expression levels of GLUT-1 and GLUT-3 in the BG in control and HI model groups (A–H), immunohistochemical staining of GLUT-1 and GLUT-3 in the BG within 72 hours after HI (I), and correlation with BG/OC (J and K). A–D, GLUT-1 expression in the control group and at 6, 24, and 48 hours after HI in the HI model groups. GLUT-1 was mainly expressed in vascular endothelial cells (positive staining is shown as dark brown, rod-shaped structures) and astrocytes (A). Positively stained endothelial cells and astrocytes increased at 6 and 24 hours (B and C) and decreased at 48 hours (D) after HI. E–H, GLUT-3 expression in the control group and at 6, 24, and 48 hours after HI in the HI model groups. GLUT-3 was mainly expressed in neurons (E). The staining of the neuronal membrane was darker at 6 and 24 hours after HI (F and G). The staining lightened, and positively stained cells decreased at 48 hours after HI (H). GLUT-1 and GLUT-3 expression levels were highest at 12–24 hours (I). Spearman correlation analysis showed that the expression levels of GLUT-1 and GLUT-3 were positively correlated with the BG/OC ratio (J and K): GLUT-1 (r = 0.64); GLUT-3 (r = 0.75).
Tables
Levels of lactate, SUVmax, MCTs, and GLUTs in the control and HI model groupsa
Parameter Control (n = 5) HI Model Group (n = 5/Group) 0–2 hr 2–6 hr 6–12 hr 12–24 hr 24–48 hr 48–72 hr Lactate 0.24 ± 0.25 7.82 ± 1.48b 16.51 ± 1.62b 13.01 ± 1.25b 3.21 ± 1.21b 1.18 ± 1.74 1.23 ± 1.40 BG/OC 0.99 ± 0.01 1.08 ± 0.04b 1.17 ± 0.06b 1.23 ± 0.02b 1.16 ± 0.03b 1.04 ± 0.04b 0.96 ± 0.01 MCT-2 0.19 ± 0.00 0.21 ± 0.01b 0.22 ± 0.01b 0.24 ± 0.01b 0.27 ± 0.01b 0.21 ± 0.01b 0.19 ± 0.00 MCT-4 0.21 ± 0.01 0.24 ± 0.01b 0.25 ± 0.01b 0.26 ± 0.01b 0.27 ± 0.01b 0.25 ± 0.02b 0.22 ± 0.02 GLUT-1 0.14 ± 0.02 0.16 ± 0.04 0.20 ± 0.05b 0.25 ± 0.01b 0.24 ± 0.03b 0.18 ± 0.05 0.15 ± 0.05 GLUT-3 0.13 ± 0.00 0.13 ± 0.01 0.16 ± 0.01b 0.22 ± 0.06b 0.18 ± 0.01b 0.14 ± 0.01b 0.14 ± 0.01
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