急性肺损伤的内皮素-1 免疫组化改变及其在发病中的作用

Immunohistochemical change of endothlin 1 in acute lung injury and the role in its pathogenesis

为了解内皮素（ＥＴ）在急性肺损伤时的作用机制，作者用Ｗｉｓｔａｒ大鼠经腹腔注射酵母多糖复制成功急性肺损伤模型测试呼吸频率及肺动脉氧分压并进行病理学免疫组化检查。结果显示呼吸频率先慢后快，氧分压下降；肺组织学显示血管内中性白细胞集聚，间质中性白细胞浸润，间质及肺泡水肿，透明膜形成，灶性出血及肺不张等改变。免疫组化显示ＥＴ－１在实验组比对照组阳性表达增强，光密度增高（即含量增高）。第一天尤其明显。ＥＴ－１含量与急性肺损伤病变的程度成平行关系作者认为，ＥＴ－１在急性肺损伤的发病机制中起着重要的作用。因ＥＴ－１为缩血管物质，故临床上应用ＥＴ抑制剂或受体拮抗剂。

on the rat acute lung injury model produced by intraperitoneal cavity injection of zymosan showed that the respiratory rate became slow at first time (1st day) ,subsequently became raped. Pulmonary histology showed that there was an accumulation of neutrophils in pulmonary microvessels,neutrophils infiltration in interstitial tissue,interetital and olveolar edema, hyaline membrane, atelectasis.Positive expression of ET 1 in experimental rats was stronger than than contral rats. Image analysis showed that OD value was elevated,especially at the fist day. The quantity of ET 1 was corresponding to the degree of pathologic change of acute lung injury. It suggests that the ET 1 might play an important role in the mechanism of acute lung injury.