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Original Article

Site-Specific Formation of Thyrotropin-Releasing Hormone-Induced Gastric Ulcers through the Vagal System

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Pages 226-231 | Received 02 Jul 1993, Accepted 04 Aug 1993, Published online: 08 Jul 2009
 

Abstract

Okumura T, Uehara A, Watanabe Y, Taniguchi Y, Kitamori S, Namiki M. Site-specific formation of thyrotropin-releasing hormone-induced gastric ulcers through the vagal system. Scand J Gastroenterol 1994;29:226-231.

The left and right dorsal motor nuclei (DMN) separately innervate the anterior and posterior gastric walls through the left and right gastric branches of the vagus nerve (GBVN) in rats. The present study was carried out to investigate the effects of selective centrally originated excitation of the unilateral vagal system on the gastric area in which vagus-induced gastric ulcers developed. Since intracisternally injected thyrotropin-releasing hormone (TRH) stimulates neurons in the bilateral DMNs to produce gastric ulcers, selective stimulation of the unilateral vagal system was produced by contralateral gastric branch vagotomy before intracisternal injection of TRH. Intracisternal injection of TRH (2 ng/rat) into left gastric branch-vagotomized rats resulted in lesion formation only on the posterior gastric wall and not on the anterior wall. In contrast, in right gastric branch-vagotomized rats TRH-induced gastric lesions were observed only on the anterior gastric wall and not on the posterior wall. These results suggest that selective stimulation of the left or right DMN induces site-specific ulcer formation through the left or right GBVN. Next, gastric acid secretion was determined in pylorus-ligated rats to examine a role of acid hypersecretion in site-specific ulcer formation caused by TRH. Of interest was that gastric acid secretion in unilaterally vagotomized rats given TRH intracisternally was significantly smaller than that in sham-operated rats given intracisternal saline, although the former rats developed gastric ulcers, whereas the latter did not. It is therefore speculated that gastric hyperacidity plays a less important role in the peripheral mechanisms of TRH-induced site-specific gastric ulceration.

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