[Abstract] [Full Text PDF] (in Japanese / 19373KB) [Members Only And Two Factor Auth.]

J.Jpn. Surg. Soc.. 61(4): 488-513, 1960


EXPERIMENTAL PEPTIC ULCER UNDER AUTONOMIC NERVOUS UNBALANCE

The 2nd Surgical Department, Yokohama University School of Medicine (Director: Prof. Mikio Yamagishi)

Tetsuro SAITO

Experimental ulcers were caused to dogs under autonomic nervous unbalance by transplantation of antrum pyloricum for the purpose to investigate the relation between autonomic nervous system and the genesis of peptic ulcer. Autonomic nervous unbalance was caused by sympathetic ganglionectomy (Th6-L2), splanchnicectomy and vagotomy. After antrum pyloricum had been transplanted into the colon as diverticulum, gastroduodenostomy was performed in Group I, gastrojejunostomy in Group II, and gastrojejunostomy following gastrectomy in Group III. The results were as follows .
1. In Group I, ulcers developed definitely more in the sympathectomized and splanchnicectomized dogs than in the controls. They were also observed a little more often in the vagotomized dogs than in the controls, or at least no inhibition was observed in the formers. Gastric acidity was remarkably high in hunger, but there was no significant difference between that in the unbalanced dogs and in the controls. In other words, there was no parallel relation between the development of ulcers and gastric acidity. Histological investigations revealed that the ulcers in the controls showed exactly the same histological appearance with that of the chronic ulcers in the human being having remarkable proliferation of granulation tissue. On the other hand, the ulcers in the unbalanced dogsaee of the sympathectomized, splanchnicectomized, and vagotomized dogs- showed similar appearance to one another's. Their cellular reaction and proliferation of granulation tissue were far less than those of the ulcers in the controls. The fact suggested that they were caused by sudden self-digestion.
2. In Group 11, all of the sympathectomized, vagotomized and control dogs had high developing rate of ulcers, and no definite difference was observed among them. Gastric acidity was remarkably high in hunger, and again no significant difference was seen among them.
3. In Group III, no ulcers developed in the controls, but they developed in fairly high rate in the sympathectomized and vagotomized dogs. There was gastric anacidity in hunger in all the cases, but a little free hydrochloric acid appeared in all of them after the injection of histamine.
4. In the controls, the development of ulcers was remarkably less in the group on which gastroduodenostomy was performed than in the group on which gastrojejunostomy was done. It was also less when gastrojejunostomy was combined with gastrectomy. On the other hand, the set-up of gastroenterostomy hardly had any relation with the development of ulcers in the unbelanced dogs. The developing rate was high uniformly, and no inhibition was observed in the vagotomized dogs.
5. The direct cause of peptic ulcers was considered to be the self-digestion of gastric juice. However, the high acidity of gastric juice was not necessarily needed for the development of ulcers under autonomic nervous unbalance.
These results proved that autonomic nervous unbalance caused weakness of tissue resistance at the gastric wall, and made the foundation for ulcers to develop easily. The author believed that autonomic nervous unbalance, especially by sympathectomy played an important role in the development of ulcers.
(Auther's abstract)


<< To previous pageTo next page >>

To read the PDF file you will need Adobe Reader installed on your computer.