【摘要】 目的　为探讨急性胰腺炎 (AP)发病机制与一氧化氮 (NO)的关系。方法　本文采用实验性急性胰腺炎的动物模型 ,对AP形成后不同时相的胰腺组织中一氧化氮合酶 (NOS)的基因表达进行了检测。同时检测了血清淀粉酶 ,红细胞超氧化物歧化酶 (SOD)和病理组织。结果　术后 2 4h已形成出血性、坏死型AP ,胰腺组织中iNOSmRNA在术后 4 8h达高峰 ,且增高的幅度较大。结论　在AP形成过程中 ,由于iNOS生成大量的NO ,可导致AP发生不可逆损害。因此 ,临床上可通过寻找特异性抑制i NOS试剂 ,这就为临床治疗AP开辟了新的途径更多还原

【Abstract】 Objective To study the relationship between acute pancreatitis(AP)and nitric oxide(NO) Methods AP were induced in rats (N=36)with the use of a closed duodenal loop technique ,animals were killed at the period of 24h?36h?48h after induction of AP The normal rats (N=12) were served as controls The degrees of serum amylase levels,erythrocytic superoxide dismutase levels and histopathologic alterations were investigated At the same time , the levels of nitric oxide synthase,iNOSmRNA in pancreatic tissues were measured by using RT PCR,β actin as an inner reference Results Hemorrhagic necrotizing AP induced by the time of 24h after operation was similar to that found in man As compared with control group,serum amylase levels were markedly at 24h( P <0 01) During AP iNOSmRNA was significantly increased in trend as time passed,forming a peak at the time of 48h Conclusion In the stage of AP,iNOSmRNA produced a great deal of NO to lead to irreversible injury It cleary implied to us:through taking some measures to inhibit iNOS,symptom and sign of AP could be ameliorated更多还原