多巴胺能神经元破坏导致消化性溃疡的动物模型

AN ANIMAL MODEL OF PEPTIC ULCER INDUCED BY DESTRUCTION OF DOPAMINERGIC NEURONS

报告应用神经毒物质１－甲基－４－苯基－１，２，３，６－四氢吡啶（１－ｍｅｔｈｙ１－４－ｐｈｅｎｙｌ－１，２，３，６－ｔｅｔｒａｈｙｄｒｏｐｙｒｉｄｉｎｅ，ＭＰＴＰ）从侧脑室、皮下、腹腔３种途径注入大鼠后出现了类似于人的消化性溃疡。其发病率分别为５０％～１００％７５％、１００％而且死亡率低，是研究神经递质和溃疡病关系的一个较好模型。大鼠注入ＭＰＴＰ后结合粘液量明显增加、血清胃泌素增加、总酸分泌减少、胃液游离酸分泌变化不大。提示ＭＰＴＰ致溃疡与胃酸关系不大，可能与粘膜防御机制尤其是粘液－碳酸氢盐屏障等受损有关。不同途径给药引起不同部位溃疡的现象值得进一步研究。

An animal ulcer model resembling human peptic ulcer elicited with neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP) by different routes of administration,i.e.,intracerebroventricular(i.c.v), subcutaneous(s.c)or intrapcritoneal(i.p.)injections was newly estab- lished.MPTP given in multiple daily doses by either i. c. V. ,s.c.or i.p. produced 50%～100%, 75% and 100% gastric or duodenal ulcers respectively with low mortality and was indicative of a better animal model in elucidating the correlation between neurotransmitters and ulcer diseases.This compound de- creased total gastric acid output,increased the combined mucus secretion and serum gastrin, but had lit- tle effect on secretion of free gastric acid. Thus these resuits showed that MPTP-induced gastroduodenal ulcers are possibly associated with impaired defensive ability of mucosa,especially of mucus bicarbonate barrier instead of gastric acid. However,further study is needed to demonstrate why administration of the drug in different routes produced different ulcers.