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目的 :探讨N 乙酰半胱氨酸 (N acetylcysteine,NAC)减轻脂多糖 (lipopolysaccharide ,LPS)所致的肺损伤及其机制。方法 :应用血管环张力检测技术和扫描电镜方法 ,观察了NAC对LPS引起的肺动脉反应性及肺动脉内皮细胞超微结构变化的影响 ;并测定了肺动脉组织中丙二醛 (malondialhyde ,MDA)、超氧化物歧化酶 (superoxidedismutes ,SOD)及一氧化氮 (nitricoxide,NO)的变化。结果 :LPS(4μg/ml,7h)可降低肺动脉对乙酰胆碱 (ACh)介导的内皮依赖性舒张反应 ,NAC(0 .5mmol/L)可逆转此种反应降低而对正常肺动脉舒缩反应无明显影响 ;NAC可改善LPS引起的肺动脉内皮细胞超微结构损伤并可逆转LPS引起的肺动脉组织中MDA、NO含量增高和SOD活性降低。结论 :NAC可通过抗氧化作用保护肺动脉内皮细胞并增强肺动脉内皮依赖性舒张反应 ,提示此可能是其发挥抗肺动脉压增高从而改善内毒素所致肺损伤的机制之一。
Objective: To investigate the effects of N acetylcysteine (NAC) on lung injury induced by lipopolysaccharide (LPS) and its mechanism. Methods: The effects of NAC on the pulmonary arterial reactivity induced by LPS and the ultrastructure of pulmonary artery endothelial cells were observed by using vascular ring tension test and scanning electron microscopy. The changes of malondialhyde (MDA) Changes of superoxide dismutase (SOD) and nitric oxide (NO) Results: LPS (4μg / ml, 7h) decreased acetylcholine (ACh) -mediated endothelium-dependent vasodilatation in pulmonary arteries. NAC (0.5mmol / L) reversed this response and had no obvious effect on normal pulmonary artery vasoconstriction NAC can improve the LPS-induced pulmonary arterial endothelial cell ultrastructure damage and can reverse LPS-induced increase in pulmonary artery tissue MDA, NO content and SOD activity decreased. CONCLUSION: NAC can protect pulmonary artery endothelial cells and increase pulmonary endothelium-dependent vasodilatation through antioxidation, suggesting that NAC may be one of the mechanisms of its anti-pulmonary vascular pressure increasing to improve endotoxin-induced lung injury.