[Bile secretion induced by L-thyroxine and substance P in dogs]. / Zhelcheotdelenie u sobak pod vliianiem L-tiroksina i substantsii P.

I.M. administration of L-thyroxin activated hepatic secretory function and changed the bile chemical contents. The substance P intensified production of bile and increased the absolute contents of free and conjugated bile acids, cholesterine, bilirubin, and total protein in the bile.

[The effect of lactin on histamine-stimulated gastric secretion and choleresis]. / Vliianie laktina na stimulirovannuiu gistaminom zheludochnuiu sekretsiiu i kholerez.

Lactine was found to depress the level of the histamine secretion of the gastric juice and to reduce the debit of hydrochloric acid in dogs. This peptide suppressed mainly the spontaneous choleresis and alters the compound composition of the bile. Large doses of the hormone obviously suppress the transport of bilirubin into the secret.

[Effect of H1- and H2-histamine receptor blockaders on lesions of the gastric mucosa evoked by exogenous histamine in guinea pigs]. / Vliianie blokatorov H1- i H2-gistaminovykh retseptorov na vyzvannye ékzogennym gistaminom porazheniia slizistoi obolochki zheludka u morskikh svinok.

It was demonstrated in experiments on guinea pigs with the use of a histamine model of ulcerogenesis that blocking agents of H1-histamine receptors produced a more marked gastro-protective effect than H2-antagonists. The results of the study confirm the hypothesis that histamine-induced ulceration of the gastric mucosa occurs through the mediation of H1-receptors. H2-histamine receptors play a secondary role in this process.

[Effects of serotonin and stress on the state of the gastric mucosa in rats with the intact and transsected vagus nerve]. / Vliianie serotonina i stressa na sostoianie slizistoi obolochki zheludka u krys s intaktnymi i pererezannymi bluzhdaiushchimi nervami.

In experiments on vagotomized and intact rats with the use of two models of experimental gastric ulceration (injection of serotonin and stress) it was demonstrated that the inhibitory action of vagotomy on haemorrhagic gastric effectiveness was more pronounced in stress than after serotonin application. Vagotomy decreased stress-induced erosive lesions but increased serotonin-induced erosions that may be a result of the increase of gastric tissue sensitivity to this amine which developed simultaneously with significant decrease of its level in gastric wall after vagotomy. Serotonin-antagonist peritol decreased stress-induced gastric disturbances in vagotomized rats more significantly than in intact rats; this suggested the great role of serotonin in anti-ulcerogenic effect of vagotomy.

[Effect of blockaders of biogenic amine receptors on experimental ulcer development]. / Vliianie blokatorov retseptorov biogennykh aminov na éksperimental'nyi ul'tserogenez.

The effects of serotonin antagonist peritol, cholinolytic atropine, H2-receptor blocker cimetidine and dopaminergic receptor blocker metoclopramide on stress- and exogenous serotonin-induced gastric ulcerogenesis in rats were studied. Peritol was shown to inhibit significantly serotonin- an stress-induced hemorrhagic effect. Similar but less pronounced inhibit produced by metoclopramide and cimetidine. Atropine decreased gastric hemorrhages induced by serotonin but failed to affect stress-induced hemorrhagic lesions. All antagonists tested decreased stress-induced erosions. Erosive lesions stimulated by exogenous serotonin were significantly decreased by atropine only. Metoclopramide known for its cholinomimetic action increased serotonin-induced erosions. It was concluded that serotonin plays an essential role in the pathogenesis of gastric lesions, and its effects suggest the involvement of acetylcholine, histamine and dopamine.

[Changes in the energy resources of rat gastric mucosa exposed to dopamine agonists and antagonists in conditions of experimental stress]. / Izmeneniia énergeticheskikh resursov slizistoi obolochki zheludka krys pod vliianiem dofaminovykh agonistov i antagonistov v usloviiakh éksperimental'nogo stressa.

Changes in adenyl nucleotide and glycogen content in rat gastric tissue under the action of stressogenic factor and injection of the dopamine blocker metoclopramide and the dopamine precursor L-DOPA were investigated with the use of the "social stress" method devised by the authors. It was established that stress induced gastric mucosal lesions and reduced the content of adenyl nucleotides and glycogen in the gastric tissue. Preliminary injection of L-DOPA potentiated the effect of stress while metoclopramide inhibited it. The data show a role of energy balance disturbances in the gastric tissue in the pathogenesis of an acute ulcer. In the authors' opinion, the disturbances seen during immobilization psychogenic stress were caused by undue stimulation of central dopamine receptors.

[Role of dopamine receptors in the mechanism of formation of stress-induced stomach lesions]. / Uchastie dofaminovykh retseptorov v mekhanizme vozniknoveniia stressornykh porazhenii zheludka.

Experiments on rats with the use of different exposures to stress (generalized electrization and "social stress") have demonstrated that stimulation of dopamine receptors localized in the central nervous system is one of the reasons for stress-induced gastric lesions, particularly for massive hemorrhages. Stimulation of peripheral dopamine receptors seems to have a gastroprotective action. As judged from the intensity of the effects of the dopamine agonists, apomorphine and L-DOPA, on stress-induced lesions of the gastric mucosa, stimulation of D2- rather than of D1-dopamine receptors is of greater importance in stress.