一氧化氮在胃食管反流病发病机制中的作用

Effect of nitric oxide on pathogenesis in patients with gastroesophageal reflux disease

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PC polygraf HR高分辨多通道测压系统检测GERD患者的食管下括约肌压力(LESP)、食管下括约肌长度(LESL)及食管远端蠕动幅度等动力参数;应用Digitrapper MKⅢ动态食管pH监测仪检测其24h食管内pH各项参数;应用硝酸还原酶法测定血清NO含量。 结果 与对照组比较,Savary Miller Ⅰ,Ⅱ,Ⅲ级GERD患者的LESP均显著降低(分别为1.1kPa±0.1kPa,1.1kPa±0.06kPa,1.0kPa±0.08kPa,P均<0.01);Savary Miller Ⅰ,Ⅱ,Ⅲ级GERD患者的食管下段蠕动幅度也均显著降低(分别为7.7kPa±1.1kPa,7.2kPa±1.3kPa,6.9kPa±1.2kPa,P均<0.01);GERD患者的食管内24h pH值明显高于对照组;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的致病机制。

AIM To investigate the effect of nitric oxide (NO) on pathogenesis in patients with gastroesophageal reflux disease (GERD).METHODS LES pressures (LESP), LES length (LESL) and the distal esophageal peristalsis amplitude were determined by using PC polygraf HR manometry testing system; 24-hour pH of esophagus was determined by Digitrapper MK Ⅲ ambulant monitor; and serum NO concentration was also measured. RESULTS As compared with controls, LESP in patients with GERD (Savary Miller Ⅰ , Ⅱ and Ⅲ) was significantly lower (l.lkPa±0.1kPa, 1.1kPa±0.06kPa, 1.0kPa± 0.08kPa, all P<0.01); the peristaltic amplitude of lower esophagus in patients with GERD (Savary Miller Ⅰ ,Ⅱ and Ⅲ) were significantly lower (7.7kPa±1.1kPa, 7.2kPa± 1.3kPa, 6.9kPa±1.2kPa, all P<0.01). The 24-hour pH-metry in patients with GERD was higher than in controls. Serum NO level in patients with reflux esophagitis was significantly higher in comparison with that of controls. CONCLUSION The endogenous nitric oxide may play an important role in the pathogenesis of gastroesophageal reflux disease.