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目的 探讨一氧化氮 (NO)在胃食管反流病 (GERD)发病机制中的作用。方法 应用PCpolygrafHR高分辨多通道测压系统检测GERD患者的食管下段括约肌压力 (LESP)、食管下段括约肌长度 (LESL)及食管远端蠕动幅度等动力参数 ;应用Digitrap perMKⅢ动态食管PH监测仪检测其 2 4小时食管内PH各项参数 ;应用NADPH -d组化染色观察食管一氧化氮合酶 (NOS)表达 ;应用硝酸还原酶法测定血清NO含量。结果 GERD患者的LESP及LESL显著低于对照组 (P <0 0 1) ;前者的食管下段蠕动幅度明显低于后者 (P <0 0 1) ;前者的食管内 2 4小时PH值明显高于后者 ;患者食管粘膜NOS呈强阳性反应 ;其血清NO含量也显著高于对照组。结论 内源性NO可能参与GERD的致病机理。
Objective To investigate the role of nitric oxide (NO) in the pathogenesis of gastroesophageal reflux disease (GERD). Methods PCpolygraf HR high-resolution multi-channel manometry system was used to detect dynamic parameters of lower esophageal sphincter pressure (LESP), lower esophageal sphincter length (LESL) and distal esophageal peristalsis in GERD patients. Digitrap perMKⅢ dynamic esophageal pH monitor 4h esophageal pH parameters; NADPH-d histochemical staining of esophageal nitric oxide synthase (NOS) expression; nitric acid reductase method for the determination of serum NO content. Results The LESP and LESL in patients with GERD were significantly lower than those in the control group (P <0.01). The former had lower creep rate in the lower esophagus (P <0.01), while the former had a significantly higher PH in 24 hours In the latter, patients with esophageal mucosal NOS showed a strong positive reaction; the serum NO content was significantly higher than the control group. Conclusion Endogenous NO may participate in the pathogenesis of GERD.