Cordier J F, Mornex J F, Lasne Y, Gérard J P, Cordier G, Creyssel R, Touraine R
Bull Eur Physiopathol Respir. 1984 Jul-Aug;20(4):369-74.
Bronchoalveolar lavage (BAL) was carried out in six patients with radiation pneumonitis, the early radiation-induced lung damage that usually leads to radiation fibrosis. Protein analysis by immuno-electrophoresis and polyacrylamide gel electrophoresis of BAL fluid revealed leakage of circulatory proteins, including high molecular weight components. Cell count of BAL fluid showed an increased number of lymphocytes; these proved to be activated on cell cycle analysis in one patient. Collagenolytic activity, assessed by degradation of radiolabelled type I human collagen, was present in BAL fluid of all six patients. The following mechanisms are therefore considered to participate in the pathogenesis of radiation-induced lung damage: 1) permeability oedema, which led to acute respiratory distress syndrome in one case of hyperacute radiation pneumonitis, 2) lymphocyte alveolitis possibly perpetuated by activated lymphocytes, and 3) release of collagenolytic enzymes in alveolar structures contributing to fibrotic processes.
对6例放射性肺炎患者进行了支气管肺泡灌洗（BAL），放射性肺炎是早期放射性肺损伤，通常会导致放射性纤维化。通过免疫电泳和聚丙烯酰胺凝胶电泳对BAL液进行蛋白质分析，结果显示循环蛋白出现渗漏，包括高分子量成分。BAL液细胞计数显示淋巴细胞数量增加；其中1例患者经细胞周期分析证实这些淋巴细胞处于活化状态。通过放射性标记的人I型胶原降解评估的胶原olytic活性在所有6例患者的BAL液中均存在。因此，以下机制被认为参与了放射性肺损伤的发病过程：1）通透性水肿，在1例超急性放射性肺炎中导致急性呼吸窘迫综合征；2）淋巴细胞性肺泡炎，可能由活化淋巴细胞持续存在所致；3）肺泡结构中胶原olytic酶的释放，促进纤维化过程。
