髓质促甲状腺激素释放激素介导大鼠轻度酸刺激引起的迷走神经依赖性适应性胃保护作用。

Medullary thyrotropin-releasing hormone mediates vagal-dependent adaptive gastric protection induced by mild acid in rats.

作者信息

Kaneko H, Kato K, Ohning G, Taché Y

机构信息

CURE/Gastroenteric Biology Center, West Los Angeles Veterans Administration Medical Center, California, USA.

出版信息

Gastroenterology. 1995 Sep;109(3):861-5. doi: 10.1016/0016-5085(95)90395-x.

DOI:10.1016/0016-5085(95)90395-x

PMID:7657115

Abstract

BACKGROUND & AIMS: Adaptive gastric protection is dependent on vagal pathways in rats. It is hypothesized that medullary thyrotropin-releasing hormone (TRH), known to regulate vagal function, is part of the brain mechanisms mediating adaptive gastric protection.

METHODS

Urethane-anesthetized rats were pretreated with either acute bilateral subdiaphragmatic vagotomy, sham operation, or intracisternal injection of purified control, TRH, or peptide YY antibody. Gastric lesions were assessed 75 minutes after orogastric administration of 1 mL of either vehicle or 0.35N HCl followed 15 minutes later by 0.6N or 1.0N HCl.

RESULTS

Injection of 0.6N and 1.0N HCl induced gastric lesions covering 23.1% +/- 2.7% and 37.8% +/- 3.3% of the corpus mucosa, respectively. Pretreatment with 0.35N HCl resulted in 67.3% and 50.5% reductions in gastric lesions induced by 0.6N and 1.0N HCl, respectively. Subdiaphragmatic vagotomy or intracisternal injection of TRH antibody increased gastric lesions induced by 0.6N HCl to 32.2% +/- 2.2% and 42.9% +/- 5.6%, respectively, and completely abolished the protective effect of 0.35N HCl pretreatment. Control or peptide YY antibody injected intracisternally did not alter the gastric protection induced by mild acid.

CONCLUSIONS

These results indicate that medullary TRH plays a role in the vagally mediated adaptive gastric protection induced by mild acid.

摘要

背景与目的

适应性胃保护依赖于大鼠的迷走神经通路。据推测，已知可调节迷走神经功能的延髓促甲状腺激素释放激素（TRH）是介导适应性胃保护的脑机制的一部分。

方法

用乌拉坦麻醉的大鼠，分别进行急性双侧膈下迷走神经切断术、假手术，或脑池内注射纯化的对照物、TRH或肽YY抗体进行预处理。在经口给予1 mL赋形剂或0.35N盐酸75分钟后评估胃损伤情况，15分钟后再给予0.6N或1.0N盐酸。

结果

注射0.6N和1.0N盐酸分别导致胃体黏膜损伤面积占比为23.1%±2.7%和37.8%±3.3%。用0.35N盐酸预处理后，由0.6N和1.0N盐酸诱导的胃损伤分别减少了67.3%和50.5%。膈下迷走神经切断术或脑池内注射TRH抗体分别使0.6N盐酸诱导的胃损伤增加至32.2%±2.2%和42.9%±5.6%，并完全消除了0.35N盐酸预处理的保护作用。脑池内注射对照物或肽YY抗体并未改变弱酸诱导的胃保护作用。