大鼠烟雾吸入性损伤肺组织浸润出血和渗出的变化

Changes in the polymorphonuclear neutrophil infiltration,hemorrhage and plasma exudation in the pulmonary tissue in rats with smoke inhalation injury

目的 探讨烟雾吸入性损伤大鼠红细胞 (RBC)、中性粒细胞 (PMN)和白蛋白从血管进入肺组织的不同机制。 方法 采用Wistar大鼠烟雾吸入性损伤模型 ,分别于伤后 1、3、6、12、2 4h处死 ,处死前 1h分别注射13 1I 牛血清白蛋白 (BSA)、99mTc PMN、99mTc RBC。经等渗盐水灌洗 ,去除体循环内血液 ,取肺组织进行γ计数并称重 ,计算单位时间内单位重量肺组织中13 1I BSA、RBC的渗出量和PMN的浸润量 ;应用磷酸邻联茴香胺法测定髓过氧化物酶 (MPO)含量。 结果 伤后 1h大鼠RBC渗出量达高峰值 ,为 (3.5 7± 0 .6 3)× 10 6个 / g,后逐步下降 ,伤后 2 4h恢复正常 ;PMN浸润量在伤后 3h明显升高 ,伤后 6h略有降低 ,但仍高于正常 ,伤后 12h再度升高 ;伤后 1h起大鼠肺组织MPO的含量逐渐升高 ,直到伤后 2 4h;伤后 1h肺组织中13 1I BSA渗出明显增高 ,6h达高峰值 ,为(16 4 .1± 5 1.7)放射性荧光闪烁计数·min-1·g-1,2 4h时仍高于正常。 结论 伤后大鼠肺组织中出血、PMN的浸润和BSA渗出均升高 ,但峰值时间不同。炎症不是红细胞渗出的前提 ,但继发性炎症反应可能是肺水肿的主要原因。

Objective To investigate the different velocity of polymorphonuclear neutrophil(PMN) infiltration, erythrocyte diapedesis and plasma exudation into the pulmonary tissue of the rats inflicted with smoke inhalation injury, so as to explore the different mechanisms of their existence in rat pulmonary tissue after inhalation injury. Methods The rat smoke inhalation injury model was employed in the study. Wistar rats were inflicted with smoke inhalation injury, and then sacrificed at 1,3, 6, 12 and 24 post injury hours (PIH). 131 I-BSA, 99 mTc-PMN or 99 mTc -erythrocytes (RBC) were injected into rat pulmonary tissue 1 hour before sacrifice. Isotonic saline was infused into blood vessel to wash out circulation blood. Then the pulmonary tissue samples were harvested for γ-value counting and then weighed. The infiltration of 131 I-BSA, 99 mTc-PMN or 99 mTc -RBC in pulmonary tissue per gram and per minute was calculated, and MPO content was measured by phosphate T-tolidine method. Results The amount of RBC diapedesis in rat lung tissue peaked at 1 PIH, decreased thereafter and approached to normal level at 24 PIH. The amount of PMN infiltration increased at 3 PIH, slightly decreased at 6 PIH but still higher than that in normal tissue, and increased again at 24 PIH. The pulmonary tissue content of MPO gradually increased from 1 PIH to 24 PIH. The pulmonary tissue content of 131 I -BSA began to increase at 1 PIH and peaked at 6 PIH, and remained higher than that in normal tissue till 24 PIH. Conclusion Even though there was remarkable postburn increase in the erythrocyte diapedesis, neutrophil infiltration and albumin exudation with different peak time points (1, 3 and 6 PIH, respectively), Inflammation seemed not to be the premise of erythrocyte diapedesis, while the secondary inflammatory reaction might be the main cause of pulmonary edema.