摘要
为探讨内源性一氧化氮 (NO)对大鼠急性坏死性胰腺炎并发肺损伤的作用及其与巯基物质的关系 ,以 5 %牛磺胆酸钠溶液胰胆管注射 ( 1mL/kg)制成大鼠急性坏死性胰腺炎并发肺损伤模型 ,以工具药L 硝基精氨酸 (L NNA)为内源性NO阻断剂 ,观察内源性NO对肺损伤程度、肺组织内巯基物质和脂质过氧化终产物丙二醛 (MDA)质量摩尔浓度的影响。结果 :牛磺胆酸钠胰胆管注射可造成大鼠急性坏死性胰腺炎并发肺损伤 ,同时肺组织内巯基物质的质量摩尔浓度降低 ,MDA的质量摩尔浓度增加。以L NNA( 1 2 .5mg/kg)阻断内源性NO后 ,肺损伤更加明显 ,同时肺组织内MDA的质量摩尔浓度也进一步增加 ,但对巯基物质的质量摩尔浓度没有影响。提示 :内源性NO具有肺保护作用 ,其保护机制可能与抗氧化应激有关 ;巯基物质可能不参与NO的肺保护机制。
To investigate the effect of endogenous nitric oxide (NO) on lung injury in acute pancreatitis in rats and its relationship to sulfhydryl compounds and lipid peroxidation. Methods: Acute pancreatitis lung injury model in rats was induced by retrograde sodium taurocholate (5%) infusion into the pancreatobiliary duct (1 mL/kg), and NG nitro L arginine ( L NNA) was used as the inhibitor of endogenous NO. The effect of endogenous NO on lung injury, lung tissue levels of sulfhydryl compounds and malonaldehyde (MDA, the end product of lipid peroxidation), were evaluated respectively. Results: Sodium taurocholate administration produced evident lung injury associated with acute necrosis pancreatitis in rats, a decrease of sulfhydryl compounds and a increase of MDA in lung tissue. Pretreatment with the NO inhibitor, L NNA(12.5 mg/kg), significantly intensified lung injury, and resulted in a further increase of lung tissue MDA, but it had no effect on the lung tissue sulfhydryl compounds. Conclusion: Endogenous NO has the effect of lung protection, and its antioxidation may be responsible, at least in part, for the protective mechanisms. Sulfhydryl compound may not be involved in NO lung protection mechanisms.
出处
《首都医科大学学报》
CAS
2003年第1期64-66,共3页
Journal of Capital Medical University
基金
北京市卫生局重点学科项目基金资助课题 ( 1998卫科扶字 11号 )
关键词
一氧化氮
肺损伤
急性胰腺炎
巯基物质
氧自由基
nitric oxide
lung injury
acute pancreatitis
sulfhydrylcompound
oxygen free radicals
