Okamoto U, Sasaki K, Nagao N, Naiki I, Nagamatsu Y
Nihon Seirigaku Zasshi. 1982;44(11):633-41.
Non-plasmin fibrinolysis enzyme was extracted from the lung and spleen of conventional rats (Thrombos. Haemostas., 1979), although the enzyme was not found in germfree rats, suggesting the possibility that the enzyme may participate in the defence mechanism of the body. The present study was made in an attempt to determine the behavior of non-plasmin fibrinolysis enzyme of the lung tissue in the DIC model of conventional rats induced by a single injection of bacterial endotoxin. The plasminogen-activator activity of the lung tissue, and the fibrinogen level, platelet count, urea nitrogen and plasminogen-activator activity in the blood were also measured. Examination of the lung tissue in the DIC rats indicated a remarkable increase in non-plasmin fibrinolysis activity and a disappearance of plasminogen-activator activity. Inhibitor studies using t-AMCHA and DFP demonstrated that the increased non-plasmin fibrinolysis activity was not derived from activated plasmin, but from serine protease. The disappearance of plasminogen-activator activity in the lung and increase of plasminogen-activator activity in the blood suggested a release of the activator from the lung into the blood due to the endotoxin injection.
非纤溶酶纤维蛋白溶解酶是从常规大鼠的肺和脾脏中提取的（《血栓与止血》，1979年），尽管在无菌大鼠中未发现这种酶，这表明该酶可能参与机体防御机制。本研究旨在确定单次注射细菌内毒素诱导的常规大鼠弥散性血管内凝血（DIC）模型中肺组织非纤溶酶纤维蛋白溶解酶的行为。还测量了肺组织的纤溶酶原激活物活性以及血液中的纤维蛋白原水平、血小板计数、尿素氮和纤溶酶原激活物活性。对DIC大鼠肺组织的检查表明，非纤溶酶纤维蛋白溶解活性显著增加，纤溶酶原激活物活性消失。使用对氨基甲基环已烷甲酸（t-AMCHA）和二异丙基氟磷酸酯（DFP）进行的抑制剂研究表明，增加的非纤溶酶纤维蛋白溶解活性并非源自激活的纤溶酶，而是源自丝氨酸蛋白酶。肺中纤溶酶原激活物活性的消失以及血液中纤溶酶原激活物活性的增加表明，由于注射内毒素，激活物从肺释放到血液中。
