摘要
成年杂种狗15只随机等分为对照组(C组)、内毒素组(E组)和内毒素加SRI 63-441(ES组)。测定给药前后血清和肺的丙二醛(MDA)含量,β-葡萄糖醛酸苷酸(β-g)活力和肺血管外水量的变化。结果:E组注射内毒素后3、6h,血清MDA分别增加到注射前的130.06±14.00％和169.16±32.940/0,血清β-g活力分别增加到注射前的191.05±86.71％和242.54±49.04％,明显高于C组和ES组。支气管-肺胞灌洗液(BALF)β-g活力、肺组织匀浆MDA含量和肺血管外水量都明显高于C组和ES组(P<0.01)。ES组与C组比较,除BALF内β-g活力高于C组(P<0.05)外,其他都无显著性差异。肺血管外水量与肺组织MDA含量、肺血管外水量与BALF内β-g活力、BALF内β-g活力与肺组织MDA含量,都密切相关(P<0.01)。提示:血小板激活因子参与内毒素休克时急性肺损伤,其诱导脂质过氧化物的生成是造成肺损伤的重要中间环节。
We investigated whether platelet-activating factor (PAF) mediates endotoxin-induced changes of lipoperoxidation, lysosomal enzyme release and increased extravascular lung water content in dogs using a specific PAF receptor antagonist, SRI 63-441. Endotoxin infusion caused an increase in serum malonyldialdehyde (MDA) from baseline (100%) to 130.04±14.00% and 169.16±32.49% and β-glucuronidase (β-g) activity to 191.05±86.71% and 242.54±49.09% at 3 and 6h, respectively. The bronchoalveolar lavage fluid (BALF) β-g activity, lung MDA and extravascular lung water also significantly increased (P<0.01). Pretreatment with SRI 63-441 markedly attenuated these changes in serum and lung except for BALF β-g activity (P<0.05). There was a significant (P<0.01) correlation between extravascular lung water and BALF β-g and between BALF β-g and lung MDA. We conclude that platelet-activating factor may play an important role in the acute lung injury in endotoxic shock, and the lipoperoxidation induced by PAF may be an importent intermediate mechanism in lung injury.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
1992年第1期34-38,共5页
Academic Journal of Second Military Medical University
基金
国家自然科学基金 No.3880399
关键词
休克
败血性
血小板
激活因子
肺
shock, septic
platelet-activating factor
malondialdehyde
lipase
pulmonary edema
dogs
