Abstract
Hypoxic brain injury is accompanied by a decrease in various functions. It is also known that obstructive sleep apnea (OSA) can cause hypoxic brain injury. This study aimed to produce a model of an intermittent hypoxic brain condition in rats and determine the activity of the brain according to the duration of hypoxic exposure. Forty male Sprague–Dawley rats were divided into four groups: the control group (n = 10), the 2 h per day hypoxia exposure group (n = 10), the 4 h per day hypoxia exposure group (n = 10), and the 8 h per day hypoxia exposure group (n = 10). All rats were exposed to a hypoxic chamber containing 10% oxygen for five days. Positron emission tomography–computed tomography (PET-CT) brain images were acquired using a preclinical PET-CT scanner to evaluate the activity of brain metabolism. All the rats were subjected to normal conditions. After five days, PET-CT was performed to evaluate the recovery of brain metabolism. Western blot analysis and immunohistochemistry were performed with vascular endothelial growth factor (VEGF) and brain-derived neurotrophic factor (BDNF). The mean SUV was elevated in the 2 h per day and 4 h per day groups, and all brain regions showed increased metabolism except the amygdala on the left side, the auditory cortex on the right side, the frontal association cortex on the right side, the parietal association cortex on the right side, and the somatosensory cortex on the right side immediately after hypoxic exposure. However, there was no difference between 5 days rest after hypoxic exposure and control group. Western blot analysis revealed the most significant immunoreactivity for VEGF in the 2, 4, and 8 h per day groups compared with the control group and quantification of VEGF immunohistochemistry showed more expression in 2 and 4 h per day groups compared with the control group. However, there was no significant difference in immunoreactivity for BDNF among the groups. The duration of exposure to hypoxia may affect the activity of the brain due to angiogenesis after intermittent hypoxic brain conditions in rats.
Highlights
In the 2, 4, and 8 h per day groups compared with the control group and quantification of vascular endothelial growth factor (VEGF)
With one way ANOVA, the mean standardized uptake values (SUVs) was elevated in the 2 and 4 h per day groups compared with the control group (p = 0.047) after one week’s rest (Figure 3)
The reactivities of the VEGF protein showed more reactivity in the 2 h per day, 4 h per day, and 8 h per day groups compared with the control group (p = 0.003)
Summary
Intermittent hypoxic exposure from obstructive sleep apnea syndrome may induce cognitive decline because of neuronal cell apoptosis in the cortex and hippocampus [3,4,5]. Especially spatial memory, after intermittent hypoxic exposure was reported in several studies [6,7,8,9,10,11]. Functional deficits were reported and the mechanism triggering these impairments was suggested to be related to neuronal apoptosis and oxygen-free radicals, which may activate a harmful process under a chronic intermittent hypoxic condition [12,13]. Some studies reported that hypoxic conditioning may Licensee MDPI, Basel, Switzerland.
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