Histopathalogical characteristics of delayed brain injury affected by hyperbaric oxygen after acute carbon monoxide poisoning in rats
- VernacularTitle:高压氧对急性一氧化碳中毒大鼠迟发型脑损伤影响的组织病理学特点
- Author:
Jinsheng LI
;
Yaoming CHANG
;
Qingbo LI
;
Xiaoping XIE
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2006;10(46):205-208,插2
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND: In clinical practice, delayed brain injury after carbon monoxide (CO) poisoning occurs in 3% to 30% of the persons who suffered carbon monoxide poisoning and is in the main presence of dementia, psychiatric symptom and extrapyramidal symptoms. At present, its pathogenesis is unclear.OBJECTIVE: To investigate the pathological damage mechanism of delayed brain injury after CO poisoning and the protective effect of hyperbaric oxygen on delayed brain injury.DESIGN: A randomized controlled animal experiment.SETTING: Staff Room of Aviation Health, Department of Aerospace Medicine, the Fourth Military Medical University of Chinese PLA.MATERIALS: This experiment was carried out in the Laboratory of Aviation Pathology and Molecular Biology, Department of Aerospace Medicine, the Fourth Military Medical University of Chinese PLA in March 2004. Totally 80 healthy male Sprague-Dawley, of clean grade, were used in this experiment. The animals were randomized into 3 groups: normal control group (n=10), model group (n=35) and hyperbaric oxygen group (n=35).The latter two groups were separately divided into 7 time points: poisoning 6 hours, 1,3,5,7,14 and 21 days, 5 rats at each time point.METHODS: In the model group, acute CO poisoning rat models were developed by placing the rats in the poisoning jar which contained the mixture of CO and air for 60 minutes. The volume faction of CO was kept at 2 500×10-6. In the hyperbaric oxygen group, modeling was the same as that in the model group. Three hours after poisoning, the rats were given 115-minute hyperbaric oxygen treatment. Pressure was 0.2 Mpa and the volume fraction of oxygen was over 0.90. The first three days after poisoning, hyperbaric oxygen treatment was conducted twice per day, then once per day, with one day of non-administration in a week. There was no intervention in the normal control group. MAIN OUTCOME MEASURES: ① The characters of pathological changes in brain tissue of rats at each time point after poisoning were detected with histopathological and immunohistochemical methods; ② Neuronal apoptosis was detected with electron microscopy and in situ TdT-mediated-dUTP nick end labeling(TUNEL).RESULTS: After rats were modeled, the rate of death was about 10%. ① In the model group, general pathological injury occurred in the brains of rats. Denatured necrosis appeared in the neurons of cerebral cortex, hippocampus, corpus striatum, cerebellum and other regions. Injuries in cerebral cortex, hippocampus and other regions were severe. Results of haematoxylin-eosin and TUNEL staining and electron microscope observation demonstrated that apoptosis occurred in hippocampal neurons. The apop totic neurons increased on the 3rd day after poisoning, reached the peak on the 7th day (P ＜ 0.01), then gradually decreased. In the hyperbaric oxygen group, the denatured necrosis of neurons in the brains was significantly lightened, and the injuries of hippocampal region of rats at each time point were significantly attenuated in comparison with model group; The number of necrotic neurons was decreased, especially on the 5th and 7th days after poisoning (P ＜ 0.01). Hyperbaric oxygen promoted the expression of Bcl-2 in hippocampus of modeled rats, especially on the 3rd and 5th days after Coexposure (P ＜ 0.01).CONCLUSION: General delayed neuronal injury is found in the acute CO poisoning rat, with the presence of delayed neuronal necrosis and apoptosis. Hyperbaric oxygen treatment can effectively reduce denatured and necrotic neurons and promote the expression of apoptosis-inhibiting gene bcl-2, then inhibit neuronal necrosis and apoptosis.
