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目的研究内毒素(ET)致大耳白兔急性肺损伤(ALI)过程中磷脂酶A2的变化和1,6-二磷酸果糖(FDP)的拮抗作用,探讨FDP对ET所致ALI的治疗作用。方法大耳白兔随机分为对照组(A组)、ET致伤组(B组)、ET致伤+FDP干预组(C组)。A组:静脉注射生理盐水2ml/kg。B组:将内毒素按500μg/kg溶于2ml生理盐水后经颈静脉插管一次注射完毕,随后注射生理盐水1次,液体总量为2ml/kg。C组:内毒素使用剂量和方法同致伤组,随后缓慢经静脉注射FDP(300mg/kg)的生理盐水溶液,液体总量同为2ml/kg。各组分别于0h、0·5h、2h、4h及6h等不同时点测定呼吸频率、心率、血压、血气分析及血清中PLA2活性;于6h点处死动物,测定肺组织PLA2活性,并行肺组织光镜和电镜下病理学观察。结果静注ET后,B组动物与A组相比较,出现典型的ALI表现,血清和肺组织PLA2活性显著增高(P<0·01),而C组动物各项指标则介于A组和B组之间。同时,肺组织病理学观察显示,B组动物肺组织出现了明显的病理损害,而C动物肺组织的病理损害程度较轻。结论PLA2激活是ET所致ALI发病过程中重要的致伤因素。FDP可抑制PLA2激活,从而对ET所致的兔早期ALI有一定的保护作用。
Objective To investigate the changes of phospholipase A2 and fructose-1,6-diphosphate (FDP) during acute lung injury (ALI) induced by endotoxin (ET) in rabbits and explore the therapeutic effect of FDP on ALI induced by ET . Methods Large white rabbits were randomly divided into control group (A group), ET injury group (B group) and ET injury group (C group). Group A: intravenous saline 2ml / kg. Group B: The endotoxin 500μg / kg dissolved in 2ml of normal saline through the jugular vein after an injection was completed, and then injected saline once, the total amount of liquid 2ml / kg. Group C: The dose and method of endotoxin were the same as those in the injury group. Then, a solution of FDP (300 mg / kg) in physiological saline solution was slowly injected intravenously. The total amount of liquid was 2 ml / kg. Respiratory rate, heart rate, blood pressure, blood gas analysis and serum PLA2 activity were measured at different time points of 0h, 0 · 5h, 2h, 4h and 6h, respectively. Animals were sacrificed at 6h, lung tissue PLA2 activity was measured, Pathological observation under light and electron microscope. Results After intravenous injection of ET, the typical ALI appeared in group B compared with group A, PLA2 activity in serum and lung increased significantly (P <0.01), while those in group C were between group A and Between B group. At the same time, the histopathological observation of lung showed that the lung tissue of group B appeared obvious pathological damage, while the pathological damage of lung of group C was lighter. Conclusion PLA2 activation is an important factor in the pathogenesis of ALI induced by ET. FDP can inhibit the activation of PLA2, which has a certain protective effect on ET-induced early ALI in rabbits.