Plasma beta-endorphin, bombesin and pancreatic polypeptide immunoreactivity in healthy subjects and ulcer patients and changes during treatment with pirenzepine.

A lower level of BEI was demonstrated in duodenal ulcer patients in both acute and chronic cases (P less than 0.01). Treatment of patients with PI increases BEI up to values found in healthy subjects, in accordance with our previous findings (17). The basal level of BOI in ulcer patients did not differ from that in healthy subjects. A transient increase of BOI was recorded during the first phase after PI application, however, BOI decreased to basal levels at the end of the therapy (P less than 0.05). The basal PPI level was higher in both groups, primarily in acute ulcer patients (P less than 0.01). During the treatment with PI the PPI level slightly increased. Mathematical correlation between BEI and BOI, and BEI and PPI revealed a significant negative correlation (P less than 0.001). However, this correlation was found in healthy subjects only, indicating that healthy subjects with a high BEI level have lower BOI and PPI values and this relation depends on BEI. This dependence is absent in ulcer patients.

Mutual correlation between levels of plasma beta-endorphin, bombesin and pancreatic polypeptide in healthy subjects and ulcer patients.

A lower level of beta-endorphin (BE) was demonstrated in patients with both acute and chronic duodenal ulcer (P less than 0.01), while the basal level of bombesin (BO) in such patients did not differ from that in healthy subjects. The basal pancreatic polypeptide (PP) level was higher in both groups of patients, primarily in those with acute ulcer (P less than 0.01). A significantly negative correlation (P less than 0.001) between the levels of BE and BO, and between those of BE and PP, was found in healthy subjects. Similar interrelation was absent in ulcer patients.

The metabolic effects of acute and chronic administration of gastrozepin.

The structure of gastrozepin (G) resembles that of tricyclic antidepressants and antihistaminic and antiserotonic cyproheptadine which are compounds with known metabolic effects. The object of this study was to test the potential action of G on the metabolism of basic nutrients, insulin and selected hormonal parameters after parenteral administration (10 and 20 mg G) and after chronic oral administration (50 mg G) during antiulcer therapy. Investigations carried out in two groups of 7 and 9 healthy volunteers, respectively, and on one group of seven patients with ulcer disease, revealed no changes in any of the blood parameters studied, nor in the excretion of catecholamines or 17-OH steroids in the urine. Our observations practically rule out any metabotropic activity of G, thereby differentiating it from tricyclic antidepressants and cyproheptadine. Isolated significant differences from the basal value seen after G and saline, can be attributed to other than pharmacological or specific mechanisms such as stress associated with the first examination, effect of fasting, individual response of the subjects, and so on.

Plasma beta-endorphin immunoreactivity (PL-beta-ED-ir) in patients with ulcer disease and its management by acute and chronic administration of gastrozepin.

The initial level of PL-beta-ED-ir was significantly lowered in a group of 14 patients with gastroduodenal ulcer disease as compared with healthy volunteers (P less than 0.05). Immediately after i.m. administration of 20 mg gastrozepin (G) the PL-beta-ED-ir level increased but not significantly. Given orally over two weeks, G (50 mg/day) led to a more than doubling of the initial level (P less than 0.05). Controls showed no significant changes. A further meaningful change represented the time relationship of PL-beta-ED-ir during 5-hour observation to i.m. administration of 20 mg G before the start and after the end of the 2-week oral therapy. The placebo character of the above findings rules out the absence of any deviations of PL-beta-ED-ir in the diseased and healthy group after i.m. injection of saline. The study deals with the findings in relation to the pathophysiology of ulcer disease, and with a potential interference of G in the interrelation of the cholinergic and endogenous opiate systems.