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目的:探讨不同剂量高氧液(hyperoxygenated solution,HOS)对急性CO中毒脑损伤的保护作用,为临床应用提供实验依据。方法:将30只SD大鼠随机分为5组,每组6只。正常组(N组)、中毒组(C组)和中毒治疗组(H组),H组再根据输注HOS剂量不同分为,HOS 10 ml/kg(H10组)、15 ml/kg(H15组)和20 ml/kg(H20组)。C组与H组大鼠经腹腔注入CO 120 ml/kg建立中毒模型,N组给予等量空气。各组大鼠分别在输注不同剂量的液体后即刻取血0.5 ml行血气检测,1 d抽取血3 ml进行神经元特异性敏感生化指标测定。实验结束后,所有动物均在麻醉状态下切取部分脑组织制作病理切片行病理学观察。结果:CO 120 ml/kg腹腔注射1.5 h能引起严重的低氧血症。中毒后1 d神经元特异性烯醇化酶、S-100β蛋白明显升高(P<0.01)。中毒后24 h脑细胞出现明显水肿、间质增宽。中毒治疗组在静脉输注不同剂量的HOS后,动脉血氧分压(mm Hg)由43.04±4.13分别上升到69.56±3.41、77.11±2.49和81.65±3.85,脑组织病理学改变明显减轻,其中H20组降低最明显,具有显著的剂量依赖性。结论:HOS能明显提高CO中毒大鼠的Pa O2和动脉血氧饱和度,降低神经元特异性敏感指标的含量,对一氧化碳中毒脑损伤具有很好的保护作用,并具有剂量依赖关系。
Objective: To investigate the protective effect of different doses of hyperoxygenated solution (HOS) on brain injury induced by acute CO poisoning and provide experimental basis for its clinical application. Methods: Thirty SD rats were randomly divided into 5 groups with 6 rats in each group. (H group), H15 group (H10 group), H15 group (H15 group) and H15 group (H group) Group) and 20 ml / kg (H20 group). Rats in group C and group H were injected intraperitoneally with CO 120 ml / kg to establish model of poisoning, and group N was given equal volume of air. Rats in each group were given 0.5 ml of blood immediately after infusion of different doses of liquid and 3 ml of blood on 1 day for neuron-specific and sensitive biochemical determination. After the experiment, all the animals were cut under anesthesia to make some pathological sections of brain tissue pathology. RESULTS: Intraperitoneal injection of CO 120 ml / kg for 1.5 h caused severe hypoxemia. Neuron-specific enolase and S-100β protein were significantly increased 1 d after poisoning (P <0.01). 24 h after poisoning, brain cells showed obvious edema, interstitial broadening. After intravenous infusion of HOS, the oxygen partial pressure (mm Hg) increased from 43.04 ± 4.13 to 69.56 ± 3.41, 77.11 ± 2.49 and 81.65 ± 3.85 respectively in the poisoning treatment group, and the histopathological changes were significantly alleviated The H20 group showed the most obvious reduction with a significant dose-dependent manner. CONCLUSIONS: HOS can significantly increase PaO2 and arterial oxygen saturation in CO-poisoning rats and decrease the content of neuron-specific sensitive index, which has a good protective effect on carbon monoxide poisoning brain injury in a dose-dependent manner.