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本实验采用大鼠烟雾吸入模型,观察了预先给予别嘌呤醇对吸入性肺损伤后6h内肺微血管通透性、丙二醛生成、超氧化物歧化酶活性、肺灌洗液中蛋白浓度及白细胞计数和血清丙二醛的影响,并辅以肺脏病理检查。结果表明:别嘌呤醇对吸入伤大鼠可以显著降低肺微血管通透性,减少肺灌洗液中蛋白含量及白细胞计数,组织病理学检查也可见肺充血、出血、间质和肺泡水肿减轻,白细胞浸润减少等。别嘌呤醇在减轻肺水肿的同时,也使肺及血清丙二醛水平明显降低,而肺组织丙二醛含量的变化在伤后6h内与肺微血管通透性、肺灌洗液中蛋白含量及白细胞计数的变化在时间及程度上都一致。以上结果提示,别嘌呤醇通过抑制黄嘌呤氧化酶,减少超氧阴离子产生,从而抑制肺脂质过氧化,减轻吸入性肺损伤。
In this experiment, a rat smoke inhalation model was used to observe the effects of pre-administration of allopurinol on pulmonary microvascular permeability, malondialdehyde production, superoxide dismutase activity, and protein concentration in lung lavage fluid within 6 h after inhalational lung injury. White blood cell count and serum malondialdehyde effects, supplemented by lung pathology. The results showed that allopurinol could significantly reduce the permeability of pulmonary microvasculature, reduce the protein content and white blood cell count in lung lavage fluid, and reduce the congestion, hemorrhage, interstitial and alveolar edema in histopathological examination. Leukocyte infiltration and so on. Allopurinol reduced edema in the lungs and serum while reducing pulmonary edema. The change in MDA content in the lung tissue was associated with microvascular permeability and protein content in lung lavage fluid within 6 hours after injury. Changes in white blood cell counts are consistent in time and degree. The above results suggest that allopurinol inhibits the production of superoxide anion by inhibiting xanthine oxidase, thereby inhibiting lipid peroxidation and reducing inhaled lung injury.