摘要
狗静脉注射大肠杆菌内毒素(2mg/kg)可引起动脉血和支气管肺泡灌冼液(BALF)中血小板激活因子(PAF)含量明显增加,同时血清和BALF中磷脂酶A_2(PLA_2)活性升高,平均动脉压降低。注射后6h处死动物,发现BALF内中性粒细胞和淋巴细胞明显增多,蛋白含量升高;肺系数和肺血管外水量增加。PAF受体拮抗剂SRI 63-411可抑制内毒素引起的PLA_2活性升高,减轻内毒素性低血压和肺损伤。提示PAF是参与内毒素性肺损伤的重要介质。PAF激活白细胞释放氧自由基和溶酶体酶,是内毒素血症时肺血管壁通透性升高的重要机制之一。
Intravenous administration of E. coli endotoxin (2mg/kg) caused a persistent increase in platelet activating factor (PAF) contents in arterial blood and bronchoalveolar fluid (BALF). Meanwhile phospholipase A2(PLA2) activity in serum and BALF was elevated and mean arterial blood pressure declined. The total cell number, expecially polymorphonuclear leukocytes and lymphocytes, and protein concentration in BALF were markedly increased 6 h after endotoxin injection. Lung index and extravascular lung water content of endotoxin-treated animals were significantly highter than those of controls. Pretreatment with PAF receptor antagonist SRI 63-441 blocked the increase in PLA, activity and attenuated endotoxin-induced hypotension and acute lung injury. The results suggest that PAF mediates endotoxin-induced lung injury, and leukocyte activation by PAF and the subsequent release of oxygen metabolites and lysoenzymes are important intermediate mechanisms leading to high permeability pulmonary edema.
出处
《第二军医大学学报》
CAS
CSCD
北大核心
1992年第2期111-115,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
内毒素
肺水肿
磷脂酶A
狗
PAF
platelet activating factor, endotoxins
pulmonary edema
phospholipase A
dogs
