目的探讨细胞粘附因子-1(ICAM-1)与新生大鼠高氧肺损伤的关系以及高氧肺损伤的发病机制。方法取102只胎龄22天足月新生大鼠,随机分为实验组与对照组各51只。实验组生后立即置入持续高浓度氧(>95%)环境中饲养,对照组在空气中饲养。两组新生大鼠根据随机数字法于生后第3、7、14天各抽取8只定位相应亚组。处死新生鼠取其肺组织,HE染色观察肺组织病理变化,Masson三色染色判断肺组织纤维化程度,免疫组化检测ICAM-1并对表达强度进行半定量分析。结果 (1)对照组生后3、7、14天各亚组未见肺损伤的病理性改变,Masson三色染色未见胶原沉积增多现象,ICAM-1在肺组织中阴性或弱阳性表达。(2)实验组7天HE染色可见大量炎细胞浸润,肺间隔轻度增宽,14天炎细胞浸润减少,肺泡结构破坏较明显,肺间隔明显增厚;Masson三色染色生后7天胶原沉积开始增加,14天纤维化程度更加显著,ICAM-1在各时间点均呈阳性表达,且分布广泛;半定量分析显示,实验组各时间点ICAM-1的表达明显高于对照组,生后7天表达最强(P<0.05)。结论高氧对肺组织有明显的损害作用,高氧暴露早期ICAM-1在肺组织中的表达随着暴露时间的延长而增加,ICAM-1在高氧暴露早期的急性炎症阶段起作用,继续暴露则逐渐降低,并未证实其与高氧肺损伤后期的纤维化有关系。 Objective To investigate the relationship between cell adhesion molecule-1 (ICAM-1) and hyperoxia-induced lung injury in neonatal rats and the pathogenesis of hyperoxic lung injury. Methods Totally 102 newborns with gestational age of 22 days were randomly divided into experimental group and control group (n = 51). The experimental group was housed immediately after exposure to high concentrations of oxygen (> 95%) and the control group was housed in air. Two groups of newborn rats according to the random number method on the 3rd, 7th, 14th days after the birth, each of the eight positioning corresponding subgroups. Neonatal rats were sacrificed to take the lung tissue, HE staining was used to observe the pathological changes of the lung tissue. Masson’s trichrome staining was used to determine the degree of lung fibrosis. ICAM-1 was detected by immunohistochemistry and semiquantitatively analyzed. Results (1) Pathological changes of lung injury were not observed in the control group at 3, 7, and 14 days after birth. Masson trichrome staining showed no increase of collagen deposition. ICAM-1 expression was negative or weakly expressed in lung tissue. (2) The experimental group 7 days HE staining can be seen a large number of inflammatory cell infiltration, lung interval slightly widened 14 days of inflammatory cell infiltration reduced alveolar structure damage obvious lung thickening; Masson trichrome staining 7 days after birth collagen The deposition began to increase, and the degree of fibrosis was more significant on the 14th day. ICAM-1 was positive at all time points and distributed widely. Semi-quantitative analysis showed that the expression of ICAM-1 at each time point in the experimental group was significantly higher than that in the control group 7 days after the strongest expression (P <0.05). CONCLUSION: Hyperoxia can obviously damage lung tissue. The expression of ICAM-1 in lung tissue increases with the exposure time in the early stage of hyperoxia exposure. ICAM-1 plays an important role in the early stage of hyperoxia exposure and continues Exposure gradually decreased, and did not confirm its relationship with fibrosis in the latter part of hyperoxia-induced lung injury.