Fig 1.
Spatial distribution of oxygen in brain tissues in vivo.
(A) Sample points on the A line. The red dots indicate the sample points separated by 0.1 mm along the A line (AP, 0 mm; LR, 1.3 mm; D, 0.0~-9.0 mm). (B) The trail of microprobes on the A line. The red arrow points to the trail left by the microprobe along the A line in the brain tissue. (C) Po2 values in different encephalic regions along the A line (n = 6). Po2 values in the Cg and LV are much higher than those in other regions of the brain. (D) Sample points on the B line. The red dots indicate the sample points separated by 0.1 mm along the B line (AP, 3.6 mm; LR, 2.0 mm; D, 0.0~-6.0 mm). (E) The trail of microprobes on the B line. The red arrow points to the trail left by the microprobe along the B line in the brain. (F) Po2 values in different encephalic regions along the B line (n = 6). Po2 values in the DG, LV and 3 V are much higher than those in other regions of the brain.
Fig 2.
Po2 measurements of DG and LV in vivo under normoxia and at altitudes of 2000 and 3000 m.
(A) The yellow stars indicate the sites of oxygen measurements in the DG and LV along the A and B lines. (B) Ambient Po2 gradually decreases as altitude increases. (C) The Po2 in the DG in vivo decreased with the decline in ambient Po2. (D) The Po2 in the DG was highest under normoxia, then progressively decreased at 2000 and 3000 m. (E) The Po2 of the LV in vivo decreased with the decline in ambient Po2. (F) The Po2 of the LV was highest under normoxia and progressively declined at 2000 and 3000 m.
Fig 3.
Rat physiological parameters under normoxia and at altitudes of 2000 and 3000 m.
(A) Breath rates under different hypoxic environments. (B) Representative plot of real-time breath rate measurements under different hypoxic environments. (C) Heart rates under different hypoxic environments. (D) Representative plot of real-time heart rate measurements under different hypoxic environments. (E) Cerebral blood flow under different hypoxic environments. (F) Representative plot of real-time measurements of cerebral blood flow under different hypoxic environments. (G) Blood oxygen saturation under different hypoxic environments. (H) Representative plot of real-time oxygen saturation measurements under different hypoxic environments. **p<0.01 compared to the normoxia group; ##p<0.01 compared to the 2000 m group.
Fig 4.
HIF-1α and VEGF expression levels were increased by the 3000 m-intermittent hypoxia (IH) treatment.
(A) HIF-1α and VEGF expression in the hippocampus (HP) and sub-ventricular zone (SVZ) was much higher in the intermittent hypoxia (IH) group than in the normoxia group (Nor). (B) Statistical histograms indicating that HIF-1α expression in the HP and SVZ in the IH group was increased 1.39-fold (a) and 1.45-fold (b) relative to the Nor group, respectively; VEGF expression in the HP and SVZ in the IH group was elevated 2.06-fold (c) and 1.06-fold (d) compared with the IH group, respectively. **p<0.01 compared with the Nor group.
Fig 5.
Neurogenesis in the DG and SVZ was increased by the 3000 m-intermittent hypoxia (IH) treatment.
IH treatment increased neurogenesis in the SVZ (A, B) and DG (D, E). Statistical histograms showing that the number of BrdU-positive cells increased by 42% in the SVZ (C) and 131% in the DG (F) in the 3000 m-IH group compared with the normoxia group. *p<0.05; **p<0.01; bar = 200 μm; n = 4–5 mice per group.