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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 injection of E. coli endotoxin (2 mg / kg) in dogs resulted in a significant increase of platelet-activating factor (PAF) in both arterial blood and bronchoalveolar-lavage fluid (BALF), and increased phospholipase A2 (PLA2) activity in serum and BALF , Mean arterial pressure decreased. Animals were sacrificed 6 hours after injection, and the neutrophils and lymphocytes in the BALF were significantly increased and the protein content was increased. The pulmonary coefficient and pulmonary extravascular volume were increased. PAI receptor antagonist SRI 63-411 can inhibit endotoxin-induced PLA 2 activity, reduce endotoxin hypotension and lung injury. Tip PAF is an important mediator of endotoxin-induced lung injury. PAF activation of leukocytes release of oxygen free radicals and lysosomal enzymes, endotoxemia is one of the important mechanisms of pulmonary vascular wall permeability increased.