Miyashita M, Onda M, Matsuda T, Moriyama Y, Takizawa T, Kim D Y, Matsuda N, Kawanami O
Kokyu To Junkan. 1989 Jan;37(1):65-70.
Endotoxin shock was made in guinea pigs to understand the initial pathogenesis in connection with the oxygen radicals from leukocytes. The intraperitoneal injection of LD50 E. coli endotoxin induced rapid leukopenia, and leukocytosis appeared at 24 hours of injection. The cell differential counts of bronchoalveolar lavage fluid revealed a significant increase in eosinophil at 10 and 30 minutes. There was also a significant increase in neutrophil at 24 hours. The activity of superoxide dismutase in the lung tissue decreased at 10 minutes of injection and remained low for 24 hours. Malonaldehyde, a lipid peroxidation metabolite by oxidants, gradually increased and reached a maximal value at 60 minutes of injection. The lung damage was histologically characterized by a rapid appearance of the alveolar edema and scattered infiltration of granulocytes. These suggested the endotoxin injection induced activation of granulocytes recruited from peripheral blood to cause oxidant reaction in lung tissues, which finally produced acute lung injury.
通过在豚鼠身上制造内毒素休克来了解与白细胞氧自由基相关的初始发病机制。腹腔注射半数致死量的大肠杆菌内毒素会导致白细胞迅速减少,注射24小时后出现白细胞增多。支气管肺泡灌洗液的细胞分类计数显示,注射后10分钟和30分钟嗜酸性粒细胞显著增加。24小时时中性粒细胞也显著增加。肺组织中的超氧化物歧化酶活性在注射后10分钟降低,并在24小时内保持较低水平。丙二醛是氧化剂引起的脂质过氧化代谢产物,逐渐增加并在注射后60分钟达到最大值。肺损伤的组织学特征是肺泡水肿迅速出现和粒细胞散在浸润。这些表明内毒素注射诱导外周血募集的粒细胞活化,导致肺组织中的氧化反应,最终产生急性肺损伤。