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探讨急性胰腺炎（ＡＰ）发病机制与一氧化氮（ＮＯ）的关系，用十二指肠闭拌法诱导大鼠实验性ＡＰ模型，并对ＡＰ形成后检测不同时相的胰腺组织一氧化氮合酶（ＮＯＳ）ｍＲＮＡ，以了解ＡＰ病程中ＮＯＳ基因表达水平的动态变化。４８只大鼠随机分四组。一组为对照组，三组为实验组。实验组分别于术后２４、３６、４８ｈ处死检测血清淀粉酶，取胰腺组织进行逆转录聚合酶链反应（ＲＴ—ＰＣＲ），检测ＮＯＳＣＤＮＡ含量。结果：术后２４ｈ已形成出血坏死型ＡＰ，血清淀粉酶比对照组显著增高（Ｐ＜０．０１），而ＮＯＳｍＲＮＡ水平与对照组相比无明显改变。至３６ｈ时ＮＯＳｍＲＮＡ水平显著增高至对照组的１．２或１．５倍（Ｐ＜０．０１），其后又开始下降。结论：大鼠实验性ＡＰ胰腺组织ＮＯＳ基因表达在术后３６ｈ达高峰，４８ｈ时下降，ＮＯ在ＡＰ发病过程中有一定作用，其确切机理有待进一步探讨。
To investigate the relationship between the pathogenesis of acute pancreatitis (AP) and nitric oxide (NO), the rat experimental AP model was induced by closed duodenum decoction and the expression of nitric oxide Synthase (NOS) mRNA to understand the dynamic changes of NOS gene expression in AP course. 48 rats were randomly divided into four groups. One for the control group, three for the experimental group. Serum amylase was detected at 24, 36 and 48 hours after operation in experimental group, and pancreatic tissues were taken for reverse transcription polymerase chain reaction (RT-PCR) to detect the content of NOSCDNA. Results: Hemorrhagic necrosis type AP was formed at 24 hours after operation, serum amylase was significantly increased (P <0.01), while NOS mRNA level was not significantly changed compared with the control group. The level of NOS mRNA increased to 1.2 or 1.5 times (P <0.01) at 36h, then decreased again. CONCLUSION: The expression of NOS gene in rat pancreatic tissue reaches the peak at 36h after operation and decreases at 48h. NO plays a role in the pathogenesis of AP. The exact mechanism remains to be further explored.