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目的探讨一氧化碳(CO)中毒迟发性脑损伤的病理机制,及高压氧治疗对迟发性脑损伤的作用,为临床治疗提供实验依据。方法参照Ischiropoulos的方法制备急性CO中毒动物模型。采用组织病理学、免疫组织化学等方法检测大鼠染毒后1、3、5、7、14、21d等各时间点脑组织病理改变的特点并与高压氧治疗组比较,以此评价高压氧的治疗作用。通过原位末端转移酶标记(TUNEL)技术方法进行细胞凋亡的检测,观察急性CO中毒及高压氧治疗后神经元凋亡的发生情况。结果急性CO中毒大鼠脑内发生广泛的病理损伤,中毒组大鼠脑皮质、海马和纹状体等部位神经元出现变性坏死,其中大脑皮质、海马等部位损伤较重。TUNEL染色表明,CO中毒大鼠海马神经元发生凋亡,凋亡神经元从染毒后第3天开始显著增加,第7天达到高峰(P<0.01),以后逐渐减少。CO中毒动物,高压氧治疗组与非治疗组比,脑内神经元变性坏死明显较轻,各时间点海马区损伤均较轻;凋亡神经元数目较少,尤以CO中毒后第5天和第7天明显(P<0.01)。高压氧促进CO中毒大鼠海马区Bcl-2蛋白表达,尤以CO暴露后第3、5天明显(P<0.01)。结论急性CO中毒大鼠出现广泛的迟发性神经元损伤,表现为迟发的神经元坏死和凋亡。高压氧治疗可以有效减少神经元变性坏死,促进凋亡抑制基因Bcl-2表达,从而抑制神经元坏死和凋亡。
Objective To investigate the pathological mechanism of delayed brain injury induced by carbon monoxide (CO) poisoning and the effect of hyperbaric oxygen therapy on delayed traumatic brain injury, and provide experimental evidence for clinical treatment. Methods According to the method of Ischiropoulos, an animal model of acute CO poisoning was prepared. Histopathology and immunohistochemical methods were used to detect the pathological changes of brain tissue at 1, 3, 5, 7, 14, 21 days after exposure to the rats and compared with the hyperbaric oxygen therapy group to evaluate the effects of hyperbaric oxygen Therapeutic effect. Apoptosis was detected by TUNEL method and the apoptosis of neurons was observed after acute CO poisoning and hyperbaric oxygen therapy. Results Acute CO poisoning occurred extensively in the brain of rats. The neurons in the cerebral cortex, hippocampus and striatum of rats in the poisoning group were degenerated and necrotic. The damage of the cerebral cortex and hippocampus was heavier. TUNEL staining showed apoptosis of hippocampal neurons in CO poisoning rats. The number of apoptotic neurons increased significantly from the 3rd day after exposure and reached its peak on the 7th day (P <0.01), then gradually decreased. CO poisoning animals, hyperbaric oxygen treatment group compared with non-treatment group, brain degeneration and necrosis of neurons was significantly lighter, at each time point of injury in the hippocampus were lighter; fewer apoptotic neurons, especially CO poisoning after 5 days And obviously on day 7 (P <0.01). Hyperbaric oxygen promoted the expression of Bcl-2 protein in hippocampus of CO poisoning rats, especially in the 3rd and 5th days after CO exposure (P <0.01). Conclusion Acute CO poisoning in rats with extensive delayed neuronal damage, manifested as delayed neuronal necrosis and apoptosis. Hyperbaric oxygen therapy can effectively reduce neuronal degeneration and necrosis and promote the expression of apoptosis-inhibiting gene Bcl-2, thereby inhibiting neuronal necrosis and apoptosis.