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目的建立血栓栓塞1周的犬肺栓塞(PTE)模型,观察该模型缺血-再灌注后不同时间点血清肿瘤坏死因子-α(TNF-α)的变化、肺泡腔内中性粒细胞(PMN)计数及吸入20ppmNO对其影响。方法对上述PTE犬行取栓术,酶联免疫吸附试验(ELISA)法检测对照组、缺血组、再灌注前、再灌注后2、4、6h及吸入NO组血清TNF-α含量(pg/ml,下同)的变化及各组术后6h肺泡腔PMN数量变化。结果再灌注组再灌注6h后血清TNF-α含量高于再灌注前及再灌注2h(8.90±1.43vs5.67±1.43,6.54±1.53,P<0.05);吸入NO组较再灌注组TNF-α含量有减少趋势(7.28±1.49vs8.90±1.43,P>0.05);再灌注6h后,再灌注组血清TNF-α浓度高于sham组及缺血组(8.90±1.43vs5.44±1.58,6.28±0.94,P<0.05);再灌注组肺泡腔PMN数(单位:/10HPF,下同)高于缺血组及Sham组(31±11vs8±4,1±1,P<0.05);吸入NO组肺泡腔PMN数低于再灌注组(19±6vs31±11,P<0.05)。结论血清TNF-α及PMN参与了该PTE犬模型的再灌注肺损伤;吸入20ppmNO可通过降低血清TNF-α含量及减少PMN向肺泡腔的渗出而减轻再灌注损伤的炎症反应。
Objective To establish a one-week model of canine pulmonary embolism (PTE) in dogs with thromboembolism and to observe the changes of serum tumor necrosis factor-α (TNF-α), alveolar neutrophil (PMN) ) Count and inhalation of 20ppmNO impact. Methods The PTE dogs were subjected to thrombectomy and the serum levels of TNF-α in the control group, ischemia group, before reperfusion, at 2,4,6 h after reperfusion, and after inhalation of NO were measured by enzyme linked immunosorbent assay (ELISA) / ml, the same below) changes and the number of alveolar PMN 6h after operation in each group. Results The level of TNF-α in serum of reperfusion group was higher than that before reperfusion and 2h after reperfusion (8.90 ± 1.43 vs 5.67 ± 1.43, 6.54 ± 1.53, P <0.05) (7.28 ± 1.49vs8.90 ± 1.43, P> 0.05). After 6h of reperfusion, the concentration of TNF-α in reperfusion group was higher than that in sham group and ischemia group (8.90 ± 1.43vs5.44 ± 1.58 , 6.28 ± 0.94, P <0.05). The number of PMN in reperfusion group was higher than that in ischemic group and Sham group (31 ± 11 vs8 ± 4, 1 ± 1, P <0.05). The number of PMNs in alveolar spaces in inhaled NO group was lower than that in reperfusion group (19 ± 6 vs. 31 ± 11, P <0.05). Conclusions Serum TNF-α and PMN are involved in reperfusion lung injury in this PTE model. Inhalation of 20 ppm NO can reduce the inflammatory reaction of reperfusion injury by decreasing the level of serum TNF-α and reducing the exudation of PMN to the alveolar space.