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The effects of alveolar macrophage depletion by liposome technique on LPS-induced lung injury.

脂质体技术耗竭肺泡巨噬细胞对 LPS 诱导的肺损伤的影响。

基本信息

批准号：
10671454
负责人：
KAMOCHI Masayuki
金额：
$ 1.41万
依托单位：
University of Occupational Environmental Health (UOEH)
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10671454/
关键词：
lung injury endotoxin sepsis C12MDP vascular permeability liposome chlodronate エンドトキシン

项目摘要

The liposome of Cl2MDP was made using rotary evaporator. The C12MDP was a kind gift from Dr. Esser (Boeringer-Manheim).At first we examined the effect of the depletion of the alveolar macrophages on LPS-induced lung microvascular permeability in the rat. The alveolar macrophages were depleted by the intratracheal injection of the liposome of C12MDP. The control animals were injected PBS-liposome intratrachealy.We found that the LPS-induced lung microvascular permeability of the rat with depleted alveolar macrophages was significantly lower than that of the control animal at 24h after i.p. LPS injection. When we injected the liposome of C12MDP intravenously, the number of the alveolar macrophages of the rat did not change, on the other hand the intravascular macrophage (monocyte) were completely depleted.The LPS-induced lung vascular permeability of the rat with depleted intravascular macrophages was significantly higher than the control animal.In these experiments, we concluded that the alveolar macrophages play an important role in sepsis induced lung injury. However, we could not know the reason why the lung vascular permeability increased in the rat with depleted intravascular macrophages by intravenous injection of the liposome of C12MDP. The mechanism of the increase of the lung vascular permeability in the rat injected C12MDP intravenously is now under investigation.

采用旋转蒸发器法制备了Cl2MDP脂质体。C12MDP是Esser(Boeringer-Manheim)博士赠送的礼物。首先，我们研究了肺泡巨噬细胞枯竭对内毒素诱导的大鼠肺微血管通透性的影响。气管内注射C12MDP脂质体使肺泡巨噬细胞耗尽。对照组大鼠气管内注射PBS脂质体，发现肺泡巨噬细胞耗竭后24小时，肺泡巨噬细胞耗竭组大鼠肺微血管通透性明显低于对照组。注射脂多糖。静脉注射C12MDP脂质体后，大鼠肺泡巨噬细胞数量无明显变化，而血管内巨噬细胞(单核细胞)则完全耗竭，血管内巨噬细胞耗竭的大鼠肺血管通透性明显高于对照组，提示肺泡巨噬细胞在脓毒症肺损伤中起重要作用。然而，静脉注射C12MDP脂质体对血管内巨噬细胞耗竭的大鼠肺血管通透性增加的原因尚不清楚。静脉注射C12MDP后大鼠肺血管通透性增加的机制正在研究中。