Cao J, Zhang L H, Wang W L, Wang Y G, Li C F, Zhao Y X, Liu Y J
Department of Otorhinolaryngology, Peking University People's Hospital, Peking University, Beijing 100044, China.
Zhonghua Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2019 Dec 7;54(12):912-918. doi: 10.3760/cma.j.issn.1673-0860.2019.12.006.
To establish a New Zealand rabbit animal model of laryngopharyngeal reflux disease (LPRD) using esophageal balloon together with metal internal stent dilation and to investigate the changes of mucosa. 20 New Zealand rabbits were randomly divided into experimental group and control group, with 10 in each group. Balloon dilatation and metal internal stent dilation were carried out in experimental group to reproduce the animal model of LPRD.The middle of balloon was placed at the lower esophageal sphincter (LES) while the stent was placed at the upper esophageal sphincter (UES). The guide wire was placed in the control group, but the balloon was not expanded and the stent was not placed. The general condition, pH value of hypopharynx, laryngeal histopathology and changes of pepsin content of New Zealand rabbits were observed regularly. The difference between experimental group and control group was compared. The 24-hour Dx-pH monitoring results showed that the number of reflux episodes(20.0[9.5, 35.0], 13.0[6.5, 22.0]), and the percent time below pH 5.5 (1.36%[0.60%, 4.57%], 1.36%[0.43%, 2.77%]) in the experimental group at the 2nd and 4th week were significantly different from those in the control group (0[0,3.0], 1.0[0.5, 3.8]; 0[0, 0.01%], 0[0, 0], respectively, all <0.01), suggesting that the experimental group New Zealand rabbits developed LPRD. Compared with the control group under microscope, lymphocytes infiltration and submucosal gland hyperplasia increased in the mucosa of the throat of the experimental group. The results of pepsin immunohistochemical staining between the two groups were statistically significant (0.014). The use of balloon dilatation of the LES combined with metal stent dilatation of the UES can successfully establish a laryngopharyngeal reflux model, and lesions in the throat tissue can be observed.
采用食管球囊联合金属内支架扩张法建立新西兰兔喉咽反流病（LPRD）动物模型，并观察黏膜变化。将20只新西兰兔随机分为实验组和对照组，每组10只。实验组采用球囊扩张和金属内支架扩张法建立LPRD动物模型，球囊中部置于食管下括约肌（LES）处，支架置于食管上括约肌（UES）处。对照组仅置入导丝，但不扩张球囊和放置支架。定期观察新西兰兔的一般情况、下咽pH值、喉部组织病理学及胃蛋白酶含量变化，并比较实验组和对照组的差异。24小时Dx-pH监测结果显示，实验组第2周和第4周的反流发作次数（20.0[9.5，35.0]，13.0[6.5，22.0]）及pH值低于5.5的时间百分比（1.36%[0.60%，4.57%]，1.36%[0.43%，2.77%]）与对照组（分别为0[0，3.0]，1.0[0.5，3.8]；0[0，0.01%]，0[0，0]）相比，差异均有统计学意义（均P<0.01），提示实验组新西兰兔发生了LPRD。显微镜下观察，实验组兔喉部黏膜淋巴细胞浸润及黏膜下腺增生较对照组增多。两组胃蛋白酶免疫组化染色结果差异有统计学意义（P=0.014）。采用LES球囊扩张联合UES金属支架扩张可成功建立喉咽反流模型，并可观察到喉部组织病变。
