摘要
分别采用含0.03%雷尼替丁(R)的标准粉末状饲料、50μg/ml甲硝基亚硝胍(MNNG)溶液及两者联合(MNNG+R)喂饲大鼠共20周,于实验第43周末处死动物进行观察。MNNG+R组腺胃粘膜肠上皮化生诱发率及平均肠化腺体数(100.0%,696.2±173.6)显著地高于MNNG组(86.5%,330.6±145.6)或R组(22.5%、75.2±30.9)(P<0.01,P<0.05);各组大鼠幽门腺区和胃底腺区粘膜表面pH值与肠化腺体数目之间呈显著的正相关(r=0.96,r=0.99)。结果表明MNNG+R是建立大鼠腺胃粘膜肠化模型的一种理想方法;胃内高pH值可能是诱发胃粘膜肠上皮化生的主要因素之一;慢性胃病抗酸治疗的安全性还需进一步观察。
Either ranitidine (R) or N-methyl-N-nitro-N-nitrosoguanidine(MNNG) or both were administered to Wistar rats at a concentration of 0.03%in diet (R) or 50 μg/ml in drinking water(MNNG) ad libitum for 20 weeks. The rats were subsequently maintained without MNNG and/or R for an additional 23 weeks. An untreated control group was kept 43 weeks. Intestinal metaplasis (IM) was induced in the glandular stomachs of rats treated with MNNG(86.5%),R(22.5%),MNNG+R (100.0%)respectively while control group was 7.5%. There were highly significantly differences (P<0. 01,P<0. 05) between MNNG +R group and MNNG group,MNNG +R group and R group in the incidences of IM and sulphomucin positive IM, in the numbers of metaplastic glands, in pH value of gastric mucosa and its transmembranous potiential difference (PD);Apositive relation was observed between pH value of gastric mucosa and the number of metaplastic glarid (r=0. 99 in the fundic gland area, and r=0. 96 in the pyloric gland area). The results showed that :administration of both MNNG and R is a better method to induce IM of gastric mucosa in Wister rats;high pH value may be the one of main factos inducing IM of gastric mucosa;the safety of anti-acid therapy for chronic gastric diseases need to be further observed.
出处
《胃肠病学和肝病学杂志》
CAS
1995年第4期254-257,共4页
Chinese Journal of Gastroenterology and Hepatology
基金
全军"八五"重点攻关课题
关键词
胃粘膜
化生
甲硝基亚硝胍
雷尼替丁
WISTAR大鼠
gastric mucosa, metaplasia, ranitidine, N-methyl-N-nitro-N-nitrosoguanidine Wistar rats