铝碳酸镁对反流性食管炎食道粘膜保护机制的实验研究

The experimental study of Hydrotalcite′s role to the esophageal mucous membrane in reflux esophagitis

目的 观察铝碳酸镁对急性反流性食道炎的防治作用 ,并探讨其作用机制。方法 采用十二指肠结扎复制反流性食管炎模型 ,光镜下和电镜下观察大鼠食管粘膜组织学表现 ,并计算粘膜损伤指数 ,激光多普勒血流计测定粘膜血流量 ,收集胃内潴留物测定PH值及总胆酸浓度。结果 光镜下模型组大鼠食管粘膜充血水肿 ,表面明显的炎性渗出 ,严重者出现粘膜细胞的变性坏死脱落 ,形成典型的溃疡结构。治疗组大鼠部分食管粘膜下层出现炎性细胞浸润 ,局部表层粘膜上皮脱落形成糜烂灶。电镜下治疗组大鼠血管炎症反应较模型组轻 ,上皮细胞连接与对照组相比尚正常。模型组大鼠粘膜血流量较治疗组明显降低 ,其差异具有显著意义 (P <0 0 5 ) ,模型组大鼠胃潴留液量及PH值、粘膜损伤指数、总胆酸含量均较治疗组升高 ,两组相比差异具有显著意义 (P<0 0 5 )。结论 除十二指肠反流的内容物内胆酸升高外 ,局部粘膜血流量降低、胃潴留液PH值改变亦参与了反流性食管炎的形成。铝碳酸镁通过与胆酸结合 ,改善局部粘膜血流状态及调节胃内PH值而发挥其粘膜保护作用。

Aim To study the role of Hydrotalcite to the esophageal mucous membrane in reflux esophagitis.Methods SD male rats' duodenum were ligated to induce the reflux esophagitis.The esophageal mucous membrane was observed by light microscope and electron microscope,calculating the damage exponent.The mucosa blood flow was estimated by laser blood stream meter.Collecting retention of the stomach to assay its PH and total bile acid.Results Light microscopy showed model rats' esophageal mucous membranes were hyperemia and edema.Some formed the typical ulcer.Electro microscopy showed the connection of epithelial cells were still normal.The mucosa blood flow in model rats was much lower than that in controls,but the quantity of retention,PH,damage index and total bile acids were higher than that in controls( P <0 05).Conclusions Except for the high total bile acids and the local mucosa blood flow,the alteration of the PH of the retention take part in the formation of the reflux esophagitis.Hydrotalcite can bind the bile acids,improve the local mucosa blood flow,regulate the PH in the stomach,so it can protect the esophageal mucous membrane.