摘要
为探讨内源性一氧化氮(NO)对实验性急性坏死性胰腺炎的作用及其与胰腺组织磷脂酶A_2(PLA_2)活性的关系,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模型,以L-硝基精氨酸(L-NNA)为内源性NO的阻断剂,观察内源性NO对胰腺损伤程度和胰腺组织PLA_2活性的影响。发现牛磺胆酸钠胰胆管注射可造成胰腺组织明显的水肿和坏死,部分大鼠发生胰腺实质内出血,但胰腺组织内PLA_2的活性并没有显著变化。以L-NNA阻断内源性NO明显加重胰腺损伤,却对胰腺组织局部的PLA_2活性没有影响。结果提示:内源性NO具有胰腺保护作用,但其保护作用可能与胰腺组织局部的PLA_2活性无关。
To investigate the effect of endogenous nitric oxide (NO) on acute necrosis pancreatitis in rats and its relationship to phospholipase A2(PLA2) activity in pancreas, acute necrosis pancreatitis 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 pancreatic injury and pancreatic tissue PLA2 activity was evaluated respectively. Results showed that Sodium taurocholate administration induced evident pancreatic tissue edema and acinar necrosis, and the intrapancreatic hemorrhage occurred in some rats. Pretreatment with the NO inhibitor, L-NNA (12. 5 mg/kg) , significantly intensified pancreatic injury, but had no effect on the PLA2 activity in pancreatic tissue. The above results suggest that endogenous NO has the effect of pancreatic protection, but it seemed that the protection is unrelated to PLA2 activity of pancreatic tissue.
出处
《首都医科大学学报》
CAS
2003年第2期158-160,共3页
Journal of Capital Medical University
基金
北京市卫生局重点学科基金
