论文部分内容阅读
用间接免疫过氧化酶法观察实验性呼吸窘迫综合征（ＲＤＳ）兔肺泡隔纤维连接蛋白（Ｆｎ），发现其染色颗粒分布散乱无序，失去正常的“串珠样结构”；沿肺泡上皮腔面排列的线条状Ｆｎ大段断裂。同时，血浆Ｆｎ持续低下，支气管肺泡灌洗液中的白蛋白及胶体渗透压升高，肺泡水肿液中发现较多Ｆｎ染色颗粒，后者可能是成人呼吸窘迫综合征（ＡＲＤＳ）晚期易发广泛肺纤维化的主要原因之一。以上结果提示，肺泡隔Ｆｎ的形态学异常在ＡＲＤＳ通透性肺水肿的发病中有重要作用；尽早保持肺泡—毛细血管膜的完整性，对于改善ＡＲＤＳ患者的最终预后有重要意义。
Indirect immunoperoxidase method was used to observe the alveolar septa fibronectin (Fn) expression in experimental respiratory distress syndrome (RDS) in rabbits. The distribution of the stained particles was disordered and the normal “beaded” structure was lost. Fn arranged in a large section of the fracture line. At the same time, plasma Fn persistently low, albumin and colloid osmotic pressure in bronchoalveolar lavage fluid increased, and more Fn-stained particles were found in the alveolar edema fluid, which may be more common in advanced stage of adult respiratory distress syndrome (ARDS) One of the main causes of pulmonary fibrosis. The above results suggest that the morphological abnormalities of Fn in alveolar septum play an important role in the pathogenesis of ARDS. To preserve the integrity of alveolar-capillary membrane as early as possible is of great significance to improve the final prognosis of patients with ARDS.