The study of the effect of the thyroid gland on the stomach began in the early years of the 20th century, after Miesowicz discovered a decrease in acid secretion in the stomach in patients with thyrotoxicosis.
The notion of the role of the thyroid gland in the regulation of gastric secretion underwent a certain evolution depending on the level of experimental technique, methods for examining the stomach, the quality of hormonal preparations used, etc. Nevertheless, at present there is no single point of view on the problem under consideration, since the published data are very heterogeneous and often controversial.
It has been shown that giving dogs small doses of thyroidin causes an increase in gastric secretion, and large doses inhibit it. This is explained by the different excitability of the neuro-glandular apparatus of the stomach, since the stimulating effect of the hormone is especially pronounced in dogs with a small ventricle according to Pavlov (while maintaining the nerve trunks) and is much less pronounced in animals with Heidenhain’s ventricles (with cut nerve pathways). In other words, the effect of thyroid hormones on the stomach is largely mediated, because it is realized by acting on the nerve paths.
Long-term administration of thyroidin to dogs causes phase states of the secretory apparatus of the stomach: within 1 month the acidity and digestibility of the gastric juice increase, followed by a decrease in these indicators. In other studies confirming these data, there is a discrepancy in terms of the acidity of gastric juice in experimental thyrotoxicosis – its invariance under these conditions is indicated.
However, there is a well-founded opinion on this subject, according to which the administration of toxic doses of thyroidin or the feeding of animals with the thyroid gland causes a drop in gastric secretion until it stops completely.
Of particular interest are the extensive studies of S. G. Genes and N. G. Lesnoy, devoted to the mechanisms of the influence of the thyroid gland on the stomach. The authors found that during the 24-hour feeding of animals with a crude thyroid gland or the administration of thyroidin, the amount of gastric secretion does not change significantly. After cessation of feeding, in conditions of decreased secretion of thyroid stimulating hormone and thyroxine (hypothyroidism condition), gastric secretion increases significantly. A prolonged increase in the acid-peptic activity of gastric juice in response to imaginary feeding or the introduction of histamine also occurs with hypothyroid goiter in dogs, which developed as a result of the daily administration of thyreostatic agents (6-methylthiouracil). Based on the assumption that the thyroid hormone exerts its effect on the body by changing the functional state of the cerebral cortex, the authors investigated the effect of the hormone on the stomach under conditions of weakening of the excitatory and inhibitory processes in the cerebral cortex caused by castration. It turned out that castrated animals are more sensitive to the introduction of thyroidin than intact ones: small doses of the hormone enhance the “histamine” gastric secretion, and large ones inhibit it. Therefore, in non-castrated dogs under conditions of hypothyroidism and in castrated dogs receiving long-term thyroidin, the secretory activity of the stomach is the same.
Inhibition of the activity of the central nervous system, as well as its direct effect on the gastric glands, is considered as the main mechanism of the inhibitory effect of the thyroid hormone on the stomach.
Removal of the thyroid gland in dogs with experimental thyrotoxicosis entails a decrease in the secretion of gastric juice. The latter usually occurs after a phase of increased gastric secretion; In the future, the secretion parameters return
to the initial level, and the thyroidin supplementation increases the activity of the gastric glands. A number of foreign authors have confirmed the inhibitory effect of experimental hypothyroidism on gastric secretion.
There is evidence of the opposite nature, according to which thyroidectomy causes a prolonged increase in gastric secretion.
Of fundamental importance is the question of the importance of the thyroid gland in the regulation of trophic processes in the mucous membrane of the gastro-duodenal region. This is due to the fact that thyroxine plays an important role in ensuring normal oxidative processes in tissues, their differentiation and recovery.
Therefore, it is natural to expect a violation of these processes in various organs and tissues (including the mucous membrane of the stomach) when the thyroid gland is turned off. However, the first studies on the state of the stomach under experimental atherosis showed moderate dystrophic changes in the secretory apparatus of the stomach without its pronounced structural reorganization.
S. M. Lipovsky, on the basis of his experiments with thyroidectomized rats, refuted this point of view. The author claims that “… after total thyroidectomy, significant histological and histochemical changes occur, expressed in the ability to slowly proceeding destruction of the most differentiated epithelial elements of the glands of all parts of the stomach.” It is also indicated that the detected changes in the distribution of RNA in the secretory cells of the gastric mucosa are responsible for the development of their dysfunction.
The administration of thyroid hormone to thyroidected animals increases the number and depth of defects in the gastric mucosa (including ulcers) when reproducing ulcers according to the Shay method.
Thyroidectomy, as well as the introduction of 6-methylthiouracil, has a protective effect on the gastric mucosa when trying to cause peptic ulceration by a similar method.
These data show that, under certain conditions, thyroid hormone is related to the development of destructive changes in the gastric mucosa.