組織トロンボプラスチン静注後にみられた塞栓性肺病変

Embolic pneumopathy induced by tissue thromboplastin

　肺胞隔膜は肺の機能を遂行する主要な場で，肺微小血栓症，肺胞蛋白症，肺胞硝子膜症，肺胞隔膜炎などに関連して，臨床的には重篤な呼吸困難を生ずる。また呼吸機能の面では肺胞—毛細管ブロック症候群を呈する特異な病態である。しかしながら，その成立機転についての検索は十分でなく，まだ明らかでないことが多い。そこで肺微小血栓症作成のため，組織トロンボプラスチンを引き金因子として家兎に静注し，肺微小血栓形成過程ならびにその消失過程と共に経時的に肺胞隔膜の変化を電顕的に観察した。

Rabbits received 25 mg/5 ml of NaCl of tissue thromboplastin. A systematic ultrastructural study was carried out after 10 sec., 1 min., 5 min., 24 hrs, 48 hrs and 1 w. 5 min. after injection of tissue thromboplastin, capillaries were obstructed by recent thrombi formed of fibrin or fibrin-platelets. As early as 24 hrs, capillary obstruction had disappeared. In the vicinity of these acute lesions, some endothelial cells were normal and some were destructive; interstitial tissues were edematous; lamellar inclusion bodies vacuolated in type II alveolar epithelial cells. After 1 w., the most striking change was the proliferation of type II cells. Moreover, the vacuolation or the disappearance of lamellar inclusion bodies was found in type II cells. These changes of lamellar inclusion bodies may lead to decrease the surfac-tant activities on alveolar walls.