摘要
目的 探讨胎粪诱导急性肺损伤的发病机制及抗氧化剂重组人超氧化物歧化酶(recombinanthumansuperoxidedismutase,rhSOD)的保护作用。 方法 32只雄性SD大鼠 ,随机取出 8只经气管置管注入生理盐水 1ml/kg作为对照 (生理盐水组 ) ,2 4只大鼠由气管置管注入 2 0 %胎粪 1ml/kg复制大鼠胎粪肺损伤模型 ,随机分为 :胎粪组 (8只 ) ;胎粪 +生理盐水组 (8只 ,气管内注入生理盐水 1ml/kg) ;胎粪 +rhSOD组 (8只 ,气管内注入rhSOD 2 0mg/ml/kg)。 2 4h后分别行大鼠支气管肺泡灌洗液 (BALF)细胞计数和蛋白含量、肺通透指数 (BALF蛋白含量 /血浆蛋白含量 ,pulmonarypermibilityindex ,PPI)、乳酸脱氢酶 (LDH) ,肺组织匀浆髓过氧化物酶 (MPO)活性和丙二醛 (MDA)、一氧化氮 (NO)含量及超氧化物歧化酶 (SOD)活性检测 ,并观察光镜下动物肺损伤的程度。结果 与生理盐水组比较 ,胎粪组和胎粪 +生理盐水组BALF细胞计数、蛋白含量、PPI、LDH及肺组织MPO活性、MDA、NO含量、肺损伤病理评分均显著增高 (P均 <0 0 1) ,肺匀浆SOD活性略有上升 ,但差异无意义 (P >0 0 5 ) ;胎粪组与胎粪 +生理盐水组比较 ,上述指标差异均无显著意义 (P均 >0 0 5 ) ;与胎粪 +生理盐水组比较 ,胎粪 +rhSOD组大鼠BALF细胞计数、LDH、肺匀浆MPO活?
Objective To evaluate the pro tective effects of recombinant human superoxide dismutase (rhSOD) in acute lung injury (ALI) following meconium aspiration. Methods Thir ty-two healthy male Sprage-Dawley rats were divided into two groups, 8 were us ed as control (saline group) by infusing 1 ml/kg saline through endotracheal tub e; the other 24 rats were used to establish model of ALI by infusing 1 ml/kg of 20% human newborn meconium suspension through endotracheal tube, and then were r andomized to 3 groups (8 each): meconium group with no administration of saline or rhSOD; meconium+saline group by infusing 1 ml/kg saline through endotracheal tube; meconium+rhSOD group by infusing 20 mg/kg rhSOD dissolved in 1 ml/kg sali ne through endotracheal tube. The rats were killed 24 h after treatment. The m easurements included bronchoalveolar lavage fluid (BALF) cell counts, protein, B ALF protein/plasma protein ( pulmonary permibility index, PPI),lactic dehydroge nase (LDH), pulmonary myeloperoxidase (MPO) and superoxide dismutase (SOD) activ ity, malonyldialdehyde (MDA) and nitric oxide (NO) level. Lung injury score was also evaluated. Results Compared with the saline group, the rats in the meconium group had significantly increased BALF cell counts (4 .04±1.01 vs. 0.53±0.19), protein (2.54±0.74 vs. 0.67±0.26) , PPI (0.50±0.18 vs. 0.12±0.05), LDH (263.50±97.84 vs. 17.38 ±3.58), pulmonary MPO (1.49±0.22 vs. 0.62±0.16), MDA (3.30±0.85 vs. 1.40±0.35), NO (12.77 ±5.00 vs. 4.89 ±1.32) and lung inju ry score (9.88±2.10 vs. 2.25±1.04), P< 0.01 for all, whereas pu lmonary SOD activity had no statistically significant differences (103.28±24. 53 vs. 94.49±12.93, P>0.05). There were no statistically significa nt differences between meconium+saline group and meconium group(all P>0.05 ). Compared with the meconium+saline group, meconium+rhSOD group had decreased BALF cell counts (3.13±0.77 vs. 4.68±1.40, P<0.01) , LDH (162. 63±76.90 vs. 273.75±111.83,P<0.05), pulmonary MPO activity (1.2 3±0.28 vs. 1.54±0.24, P<0.05), MDA (2.46±0.42 vs. 3.50± 0.82, P<0.01), NO level (9.17±2.34 vs. 13.04 ±4.38,P<0.05 ), lung injury score (8.63 ±1.30 vs. 10.00±1.07, P<0.05) and inc reased pulmonary SOD activity (134.45±23.30 vs. 106.79±17.77, P<0 .05),but there were no statistically significant differences in BALF protein a nd PPI between these two groups. Conclusion Inflammation and lipid peroxidation might play important roles in the pathogenesis of ALI wi th meconium aspiration, a single early administration of 20 mg/kg rhSOD intratra cheally can reduce lung damage in rats following meconium aspiration.
出处
《中华儿科杂志》
CAS
CSCD
北大核心
2004年第10期777-781,i002,共6页
Chinese Journal of Pediatrics
基金
浙江省卫生厅重点课题资助项目 (W 10 12 5 )
浙江省教育厅资助项目 ( 2 0 0 3 0 3 0 4)
浙江省科技厅资助项目 ( 2 0 0 4C3 3 0 19)
