Tsubouchi T
Department of Surgery, School of Medicine, Keio University, Tokyo, Japan.
Nihon Geka Gakkai Zasshi. 1990 Jun;91(6):749-59.
This study was undertaken to clarify the mechanism of the development of ARDS and to improve its treatment by studying the role of polymorphonuclear leukocytes (PMNs) in an endotoxin shock model of rats. PMNs from a rat were labeled with 111In by the use of tropolone and were injected into rats pretreated with endotoxin. Then the biodistribution of PMNs was studied by either counting the radioactivity of excised organs or using a gamma scintillation camera on the anesthetized rats. The two methods facilitated to observe the distribution of PMNs fairly a short time after the injection of endotoxin. There was a significantly higher radioactivity in the lungs of the endotoxin group than in the control group. The accumulation of PMNs into the lungs occurred immediately after endotoxin injection. In rats depleted of the complement by cobra venom factor (CVF), an increase in radioactivity in the lung was not observed. These results indicate that the complement system is involved in the pathogenesis of ARDS. When rats were injected with methylprednisolone, the pulmonary accumulation of 111In-PMNs by endotoxin were suppressed. This is an experimental support of possible beneficial effects of corticosteroids in the treatment of ARDS.
本研究旨在通过研究多形核白细胞（PMNs）在大鼠内毒素休克模型中的作用，阐明急性呼吸窘迫综合征（ARDS）的发病机制并改善其治疗方法。利用托酚酮将大鼠的PMNs用铟-111标记，然后注入经内毒素预处理的大鼠体内。之后，通过计数切除器官的放射性或在麻醉大鼠身上使用γ闪烁相机来研究PMNs的生物分布。这两种方法有助于在注射内毒素后相当短的时间内观察PMNs的分布情况。内毒素组大鼠肺部的放射性明显高于对照组。内毒素注射后，PMNs立即在肺部积聚。在用眼镜蛇毒因子（CVF）耗尽补体的大鼠中，未观察到肺部放射性增加。这些结果表明补体系统参与了ARDS的发病机制。当给大鼠注射甲基泼尼松龙时，内毒素诱导的铟-111标记的PMNs在肺部的积聚受到抑制。这为皮质类固醇在ARDS治疗中可能的有益作用提供了实验支持。
