| Objective: Oxygen therapy is often needed during neonatal treatment.Premature brain is not mature,prone to high concentration of oxygen damage,and even leave serious long-term neurological disorders.High oxygen brain injury in premature infants,hidden disease,no specific clinical performance,and there is no accurate and sensitive early diagnosis method.Positron emission omography /computed tomography(PET/CT)can be used by detecting changes in glucose metabolism in tissue,has been used in early diagnosis and prognostic evaluation of various central nervous system diseases,and can be used in early diagnosis of high oxygen brain injury is unclear.It is unclear whether glucose metabolism is altered in the onset of hyperaerobic brain injury.Based on the basis of the animal model of high-oxygen brain injury,PET/CT first detected the change of glucose metabolism of brain tissue,then discussed the value in the early diagnosis of high-oxygen brain injury,and discussed the change of long-term cognitive function after brain injury.Methods: The brain injury model of neonatal SD rats induced by hyperoxia was established.Neonatal SD rats within 12 hours after birth were randomly divided into air group and hyperoxia group.The neonatal rats in the hyperoxia group were placed in a self-made oxygen box with their mother,and oxygen was continuously supplied.The oxygen concentration monitored by the oxygen meter was maintained at 85% to 90%,and soda lime was used to absorb carbon dioxide.The newborn rats in the air group were placed in the same environment with an oxygen concentration of about 21%.Open the box every 24 hours for30 minutes,observe,weigh,exchange female rats,add food,and change the litter every 3 days.After 14 days of continuous hyperoxia exposure,8 newborn SD rats were randomly selected from each group and brain tissues were collected.6 were used to measure brain tissue water content and 6 were used for HE staining to observe brain tissue morphology.The remaining 6 animals in each group underwent PET/CT scans at 14 days and 2 months after birth to observe the changes in the glucose metabolism rate of brain tissue;and the water maze experiment was performed 28 to 32 days after birth to explore cognitive function in adolescence.Results: 1.Growth and development: With exposure to hyperoxia,the newborn SD rats in the hyperoxia group grew abnormally,and gradually appeared tremors,unstable walking,and uncoordinated limbs;while the air group was generally in good condition.After hyperoxia exposure,until adulthood,the weight of the hyperoxia group was lower than that of the air group(P<0.05).2.Changes in brain tissue water content: 14 days after hyperoxia exposure,the brain tissue water content of newborn SD rats in the hyperoxia group was higher than that in the air group(P<0.05).3.The pathological changes of brain tissue: Compared with the brain tissue of newborn SD rats in the air group,the brain cells of the hyperoxia group were disordered,the cytoplasm was lightly stained and edema,and showed pathological characteristics of brain edema.4.Brain tissue glucose metabolism:Compared with the brain tissue glucose metabolism of SD rats in the air group,the glucose metabolism rate of the whole brain,cerebrum,and cerebellum in the hyperoxia group was reduced at 14 days and 2 months after birth(P<0.05).5.Results of water maze experiment: On the 3rd to 4th day of the positioning navigation experiment,compared with the rats in the air group at the same time point,the escape latency of the rats in the hyperoxia group increased(P<0.05);during the space exploration experiment Compared with the rats in the air group,the number of times the rats in the hyperoxia group crossed the original platform was significantly reduced(P<0.05).Conclusion: Hyperoxia induced damage to the brain tissue of rats,and the glucose metabolism rate of the whole brain,cerebrum,and cerebellum was reduced,and 18F-FDG PET/CT can be used to early diagnosis and explore mechanism of neonatal high oxygen brain injury;Long-term hyperoxygen exposure to the immature brain leads to long-term cognitive dysfunction,manifested in rodents as a decline in learning and spatial memory. |
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