目的与方法 :为探索硝普钠对急性胰腺炎 (AP)的治疗作用 ,采用胰管内注射牛磺胆酸钠溶液的方法建立大鼠AP模型 ,并用外源性一氧化氮 (NO)供体硝普钠 (SNP)实验性治疗 ,动态观察AP模型复制后 (8、16、2 4、48h)血浆NO、超氧化物歧化酶 (SOD)和淀粉酶含量的变化及胰腺组织学改变。结果 :AP组血浆NO、SOD明显下降 (P <0 0 5 ) ,并持续 2 4h以上 ,血浆淀粉酶含量明显升高 (P <0 0 5 ) ,而治疗组血浆NO、SOD明显高于非治疗组 (P <0 0 5 ) ,淀粉酶含量明显下降 (P <0 0 5 )。治疗组胰腺组织病理损害明显轻于模型组。结论 :大鼠实验性急性胰腺炎时 ,血浆NO含量、SOD活性明显下降 ,早期腹腔注射硝普钠能显著升高血浆NO、SOD含量 ,降低血浆淀粉酶含量 ,减轻胰腺病损。本实验为临床急性胰腺炎的早期治疗提供一新途径 Objective: To explore the therapeutic effect of sodium nitroprusside (AP) on acute pancreatitis (AP), a rat model of AP was established by intraductal injection of sodium taurocholate solution and treated with exogenous nitric oxide (NO) donor Sodium nitroprusside (SNP) experimental treatment, dynamic observation of AP model replication (8,16,2,448h) plasma NO, superoxide dismutase (SOD) and amylase content changes and pancreatic histological changes. Results: The levels of plasma NO and SOD in AP group were significantly decreased (P <0.05), and continued for more than 24 hours, the plasma amylase content was significantly increased (P <0 05) Treatment group (P <0 05), amylase content was significantly decreased (P <0 05). The pathological changes of pancreas in treatment group were obviously lighter than those in model group. CONCLUSION: In experimental acute pancreatitis, plasma NO content and SOD activity were significantly decreased. Early intraperitoneal injection of sodium nitroprusside could significantly increase plasma NO and SOD levels, lower plasma amylase content and alleviate pancreatic lesions. This experiment provides a new way for the early treatment of clinical acute pancreatitis