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目的 :探讨一氧化氮 (NO)及血管活性肠肽 (VIP)在实验性反流性食管炎 (RE)发病机制中的作用。 方法 :18只 SD大鼠随机分为 A、B、C 3组 ,A、B两组手术造成 RE,C组采用伪开腹术。2～ 3个月时用免疫组化法及彩色图像分析仪对 3组大鼠食管组织中的 NO及 VIP含量进行定性、定量测量。结果 :A、B两组大鼠均发生 RE,A组引起有溃疡的 RE的比例比 B组高。A、B两组大鼠食管壁各层组织中 NO能和 VIP能阳性神经元和其阳性产物显著多于 C组 ,A、B两组之间无明显差别。结论 :单纯十二指肠液反流可引起 RE,其致炎作用可能较混合反流要强。实验性 RE大鼠食管组织中 NO能、VIP能阳性神经显著增加 ,提示 NO能和 VIP能阳性神经在 RE的发生机制中起了重要的作用。
Objective: To investigate the role of nitric oxide (NO) and vasoactive intestinal peptide (VIP) in the pathogenesis of experimental reflux esophagitis (RE). Methods: Eighteen Sprague-Dawley rats were randomly divided into A, B and C groups. A and B groups were treated with RE and C group with pseudo-open surgery. At 2 ~ 3 months, the contents of NO and VIP in esophageal tissue of 3 groups were qualitatively and quantitatively measured by immunohistochemistry and color image analyzer. Results: RE occurred in both groups A and B, and the proportion of RE with ulcer in group A was higher than that in group B. NO and VIP positive neurons and their positive products in the layers of esophageal wall in groups A and B were significantly more than those in group C, there was no significant difference between groups A and B. CONCLUSIONS: Simple duodenal reflux can cause RE, and its proinflammatory effects may be stronger than mixed reflux. NO and VIP positive neurons in esophageal tissue of experimental RE rats increased significantly, suggesting that NO and VIP positive neurons play an important role in the pathogenesis of RE.