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At least 19 recordsLinked to original sources
PubMed1986

Effects of cyclic nucleotides, betazole hydrochloride and acetylcholine on pepsinogen secretion from isolated rabbit gastric mucosa.

The effects of dibutyryl cyclic AMP (db-cAMP), dibutyryl cyclic GMP (db-cGMP), betazole hydrochloride (betazole) and acetylcholine (ach.) on pepsinogen secretion from isolated rabbit gastric mucosa were studied using an organ culture system. The 10(-3) M db-cAMP, but not db-cGMP of any concentration, produced a significant enhancement of pepsinogen secretion into the culture medium. In the presence of aminophylline (phosphodiesterase inhibitor), betazole stimulated pepsinogen secretion at concentrations of 10(-8), 10(-6) and 10(-4) M. The 10(-4) M betazole stimulated pepsinogen secretion most strongly (208% of control) and 10(-6) M betazole induced submaximal secretion (137% of control). Ach. stimulated pepsinogen secretion at 10(-8), 10(-6), 10(-4) and 10(-2) M. The peak secretion occurred at 10(-4) M ach. (303% of control). Betazole (with aminophylline) against a background of 10(-6) M ach. (submaximal stimulation dose), produced an intense stimulation of pepsinogen secretion at the concentrations of 10(-8), 10(-6) and 10(-4) M, and the secretion rate expressed as percent of control were 277, 350 and 329%, respectively. These responses were not considered the additive action by betazole and ach. but the potential interaction between the two agents in pepsinogen secretion. From these findings, we conclude that betazole-ach. interdependency exists in in vitro pepsinogen secretion.

Acetylcholine↗
PubMed1982

Betazole-induced GIP secretion is not mediated by gastric HCl.

Betazole, a pyrazole analogue of histamine, as well as pentagastrin and HCl stimulate GIP secretion. We have asked the question as to whether betazole acts directly or via the production of HCl. Eight normal subjects and 4 patients with achlorhydria secondary to pernicious anemia were given betazole (0.5 mg/kg) by IM injection. Another six normal subjects were also given betazole but this was preceded by 200 mgs. of the H2 receptor blocker cimetidine given IV 60 mins. previously and a slow infusion of 200 mg. cimetidine given over the next 4 hr. Our results have shown that the GIP response to betazole is maintained in achlorhydric subjects as well as during H2 blockade. The results suggest that betazole and therefore histamine may stimulate GIP directly and not necessarily via the mediation of HCl.

Achlorhydria↗
PubMed1975

[Effect of the antrum and vagus nerve on the stimulation of the rat stomach by betazol in the perfusion test].

In the perfusion model on Wistar rats the action of a single s. c. injection of betazol (Histalog) in a dose of 50 mg/kg b. w. in dependence on various types of stomach operations was studied. The following effects were observed: 1. the vagotomy shortly before the perfusion test did not reduce the effect of betazol. 2. If the vagotomy dated back at least 4 weeks, a reduction of the stimulated maximum secretion to half of the controls was seen. 3. The combination of the vagotomy with a pyloroplasty led to a reduction of the stimulated maximum acid secretion to half the amount. Futhermore, the betazol effect was shortened considerably and was demonstrable for no more than 2 h after the injection. 4. The antrectomy without vagotomy, however, casued a retardation of the answer to betazol with a maximum of the stimulated secretion in the 4th hour after s.c. injection. The dissociation of the effect of betazol caused by vagotomy or antrectomy leads to the conclusion that betazol has a direct site of action in the parietal cell and a second one in the cholinergic stimulation of the vagal system.

Animals↗
PubMed1982

Effects of betazole hydrochloride and cyclic AMP on the pepsinogen secretion by rabbit gastric mucosa in organ culture.

The effects of betazole hydrochloride, dibutyryl cyclic AMP (DB-cyclic AMP) and betazole hydrochloride plus aminophylline on pepsinogen secretion by rabbit gastric mucosa were studied in organ culture. Betazole hydrochloride alone did not stimulate pepsinogen secretion at the concentrations of 10(-8), 10(-6), 10(-5) and 10(-4) M. However, 10(-3) M DB-cyclic AMP produced a significant stimulation of pepsinogen secretion into the culture medium when compared with the control. In the presence of 3 x 10(-3) M aminophylline, betazole hydrochloride in the concentration of 10(-5) and 10(-4) M stimulated pepsinogen secretion into the culture medium, and the magnitude of this increase was 2.0- and 2.8-fold, respectively, compared with the control. Aminophylline alone could not change pepsinogen secretion into the culture medium. These results suggested that the pepsinogen secretion, stimulated by betazole hydrochloride, was mediated by cyclic AMP in the chief cells.

Aminophylline↗
PubMed1975

[Stimulation of the acid secretion of the stomach in rats with and without antrectomy in the perfusion test with betazole].

In the perfusion test of the stomach of rats the stimulation of acid secretion by betazol (Histalog) after one or repeated injections was studied. The experiments yielded the following results: 1. The i.v. injection of 20 mg/kg b.w. betazol was followed by a maximun acid secretion. 2. Another infusion two hours later intensified this effect. The same acid secretion was seen after a small initial dose (5 mg/kg b.w.) half an hour before the infusion of betazol. 3. The i.v. infusion of 30 mg/kg b.w. betazol showed in the intact rat stomach a smaller acid dsecretion response than did the dose of 20 mg/kg b.w. In comparison there was a significant higher stimulation with 30 mg/kg b.w. betzaol in the rat after a distal gastrectomy (antrectomy). 4. One s.c. injection of 50 mg/kg b.w. betazol showed a significant acid response of the parietal cells with a duration of at least 7 h on a percentage comparison.

Animals↗
PubMed1978

[The potentiation of betazol stimulated gastric acidity by prednisolone in dogs (author's transl)].

In a total of 46 dogs divided into 5 groups the acute effect of a high dose of prednisolone (40 mg/kg i.v.) on betazol stimulated gastric seccretion (5mg/kh s.c.) was investigated. There was no effect of prednisolone alone. The combination of betazol and prednisolone showed a significant potentiation of betazol stimulation. This effect was not seen after truncal vagotomy before stimulation. The mechanism is either cholinergic or an interaction in the metabolism of histamine.

Animals↗
PubMed1975

Comparison of dose-response curves between acid and pepsin to betazole hydrochloride in the dog with gastric fistula.

Secretory responses to subcutaneously or intravenously administered betazole hydrochloride of graded doses were compared between acid and pepsin in the dog with gastric fistula. Although the dose related increments in acid and pepsin outputs were parallel in the range of lower doses than 2.0 to 3.0 mg/kg body weight of betazole hydrochloride, higher doses caused in decrease in pepsin output, but did not in acid output. It was pointed out that the dose of betazole hydrochloride that stimulates acid secretion maximally dose not correspond to the maximal stimulation for pepsin secretion in the dog.

Animals↗
PubMed1981

The acid secretory response to betazole and insulin hypoglycemia after selective proximal vagotomy for duodenal ulcer.

In order to assess the result of vagotomy an insulin test is usually performed postoperatively. The insulin test, however, is associated with troublesome side-effects and potentially dangerous. Also its prognostic value as regards ulcer recurrence is doubtful. In this follow-up study of 118 patients, who had selective proximal vagotomy (SPV) performed for duodenal ulcer between 1968 and 1971, the insulin test is compared with a postoperative betazole (Histalog) test. Both tests were carried out 1-3 months after SPV. The insulin tests were classified according to Hollander. For the betazole tests the following criteria were used: the test was classified as negative if the reduction in peak acid output (PAOB) exceeded 50% or if the postoperative PAOB-value was lower than 15 mmol/h irrespective of the preoperative value. Values outside these were considered positive. At the follow-up 5-9 years after surgery, a total of 17 recurrent ulcers were diagnosed. The sensitivity and the specificity - i.e. the percentage of patients with recurrent ulceration and positive criteria respectively patients without recurrent ulcer and negative criteria - were calculated for the tests. Thus, the sensitivity and specificity for the insulin tests were found to be 53% and 84% respectively and for the betazole tests 59% and 91% respectively. The difference is thus very small and it seems that a postoperative test with a non-vagal gastric stimulant gives as good prognostic information as an insulin test after selective proximal vagotomy. However, both tests give a low sensitivity (53% resp. 59%) and therefore the prognostic value regarding ulcer recurrence is doubtful.

Adult↗
PubMed1977

Effect of betazole on serum group I pepsinogen levels: relationship to gastric acid output in unoperated and postoperative patients.

A significant association has previously been found between a betazole-induced decrease in serum group I pepsinogen (PG I) levels and a low peak acid output (PAO) in symptomatic patients with vagotomy and gastric resection or a drainage procedure. This study compares the effect of betazole on serum PG I levels and gastric acid output in 245 unoperated patients (115 duodenal ulcer, 25 prepyloric ulcer, 32 gastric ulcer, 73 nonulcer) and in 73 symptomatic postoperative patients (15 subtotal gastric resection, 28 vagotomy and gastric resection, 30 vagotomy and drainage). A negative serum PGI response (2-hr serum PG I level less than 92% of basal) occurred in 10 (4.1% of the unoperated patients and in 31 (42.5%) of the postoperative patients. Seven (70%) of the former and 29 (93.5%) of the latter patients had a PAO of less than 10 mEq per hr, indicating that a negative serum PG I response is associated with a low PAO in both unoperated and postoperative patients. The PAO was greater than 10 mEq per hr in 93.1% of the 277 patients with a 2-hr serum PG I level of more than 92% of basal. Additional studies revealed that neither aspiration of gastric juice nor perfusion of the stomach with acid altered the serum PG I response. This suggests that topical acid does not modulate the effect of betazole on serum PG I levels. Finally, a negative serum PG I response has been shown to be paradoxical, in that gastric pepsin levels have been found to increase over basal concurrently with the decrease in serum PG I levels.

Betazole↗
PubMed1974

Inhibitory effect of bromazepam on basal and betazole-stimulated gastric acid secretion in man.

Basal, as well as betazole-stimulated gastric acid secretion in man is reduced after the intravenous administration of bromazepam. In subjects staying awake, this reduction is limited to the first two 15-minute periods. The reduction is highly significant in subjects who fall asleep after receiving the drug. Natural sleep causes the same depression. The low level of acid secretion is maintained until the subjects are awakened when there is a sharp and highly significant rise. Acid secretion in subjects who fall asleep after the simultaneous administration of betazole and bromazepam is significantly higher than after the administration of bromazepam alone. Sleep causes a much greater depression of basal and betazole-stimulated acid secretion than does the benzodiazepine itself. Acid secretion was measured by continuous intragastric titration and a pH-sensitive endoradiosonde.

Adult↗
PubMed1982

The effect of intraduodenal installation of oleic acid on plasma neurotensin-like immunoreactivity and on gastric acid secretion stimulated by betazole and sham feeding in man.

Intraduodenal administration of oleic acid has previously been shown to inhibit gastric acid secretion induced by pentagastrin in man. This inhibition was dose-dependent and significantly correlated to a rise in plasma concentration of neurotensin-like immunoractivity (NTLI). Maximal inhibition occurred with a volume of oleic acid of 20 ml. In the present study intraduodenal instillation of 20 ml. of oleic acid inhibited acid secretion evoked by sham feeding in healthy subjects but did not significantly inhibit the near-maximal acid secretion stimulated by the histamine analogue betazole. The inhibition of acid secretion induced by sham feeding was the same (about 45%) as the inhibition of pentagastrin-stimulated secretion. Plasma NTLI rose significantly in both the sham feeding and betazole experiments and peaked at about 145 pM. The results are in agreement with the inhibitory characteristics of neurotensin and support the hypothesis that the inhibition of gastric acid secretion by small amounts of intestinal fat is at least partly mediated by neurotensin.

Adult↗
PubMed1975

[Effect of somatostatin on betazole-stimulated gastric secretion and carbachol-stimulated pancreatic secretion and gall bladder contraction in man(author's transl)].

The effect of somatostatin on betazole-stimulated gastric secretion and carbachol-stimulated pancreatic secretion and gall bladder contraction has been studied in seven healthy volunteers. Somatostatin (150 and 250 mug/h) inhibited dose-dependently volume of gastric juice and acid output stimulated by 16 mg betazole. Acid concentration was little affected. 500 mug/h were not more effective than 250 mug/h. Pancreatic secretion stimulated by 250 mug carbachol has been reduced by 80-90% and gall bladder contraction abolished by somatostatin infusion (200 mug/h).

Adult↗
PubMed1976

The effect of betazole on serum group I pepsinogen levels: studies in symptomatic patients with and without recurrent ulcer after vagotomy and gastric resection or drainage.

Serum group I pepsinogen (PG I) levels have been determined before and at intervals after the administration of betazole hydrochloride (Histalog) in 50 symptomatic postoperative patients, 20 with and 30 without recurrent ulcer, after either a vagotomy and gastric resection or a drainage procedure. In patients with recurrent ulcer, mean serum PG I levels increased after betazole and reached a maximum of 116.5 +/- 2.2% (SE) of basal at 2 hr; range 98.9 to 135.7%. In contrast, mean serum PG I levels decreased in patients without recurrent ulcer and reached a nadir of 75.0 +/- 4.3% of basal at 2 hr; range 46.9 to 142.4%. All 20 patients with recurrent ulcer and 5 patients without recurrence had a 2-hr serum PG I level of more than 98% of basal, while each of the remaining 25 patients without recurrent ulcer had a 2-hr level of less than 92% of basal. A 2-hr serum PG I level of more than 98% of basal was also correlated with a vagotomy and drainage, a peak acid output of more than 11 mEq per hr, and a positive insulin test, while a level of less than 92% of basal was correlated with a vagotomy and gastric resection, a peak acid output of less than 11 mEq per hr, and a negative insulin test. In addition, basal serum PG I and serum gastrin levels were significantly higher (P less than 0.001) in patients with the former type of PG I response than in those with the latter type of response. The cause of each type of response is not certain, but the data suggest that one of the determinants may be the completeness of vagotomy.

Adult↗
PubMed1988

Effect of nizatidine and cimetidine on betazole-stimulated gastric secretion of normal subjects: comparison of effects on acid, water, and pepsin.

The effect of nizatidine, a new histamine H2 receptor antagonist, on gastric secretory function of eight normal subjects stimulated with betazole, was compared with that of cimetidine. Single oral doses of 75 mg, 150 mg, and 300 mg nizatidine, 300 mg cimetidine, and a placebo were administered on separate occasions 1 h before betazole stimulation. Gastric secretions were recovered in 15-min fractions for the ensuing 2 h, and the pH, H+ concentration and output, volume, and pepsin concentration and output were determined. Doses of 150 mg and 300 mg nizatidine depressed the secretory response significantly more than did cimetidine. The antisecretory effects of 75 mg nizatidine was no different than that of 300 mg cimetidine. Nizatidine 300 mg inhibited pepsin output significantly more than volume. Although pepsin concentration was reduced more than volume, the difference was not significant. These observations, in contrast to results of previous studies, suggest a direct inhibition of pepsin secretion, although to a lesser extent than that of acid.

Adult↗
PubMed1978

Benign gastric ulcer in a patient with betazole-fast achlorhydria.

We report a case of benign gastric ulcer that occurred in a 50-year-old man with betazole hydrochloride-fast achlorhydria. The rarity of exceptions to the rule that ulcers in achlorhydric stomachs are malignant (to our knowledge, this is only the sixth reported case) confirms the wisdom of regarding such ulcers as malignant until proved unequivocally to be benign.

Achlorhydria↗
PubMed1980

The effect of antral distension in healthy subjects on betazole-stimulated gastric acid secretion and the plasma concentration of immunoreactive neurotensin.

Antral distension in seven healthy subjects had the same inhibitory effect, approximately 20% inhibition, on gastric acid secretion stimulated by pentagastrin and betazole (Histalog). The plasma concentration of neurotensin in peripheral venous blood was unchanged during antral distension in healthy subjects. The plasma concentration of neurotensin in portal blood was also unchanged during antral distension in anaesthetized duodenal ulcer patients and in non-ulcer patients. The inhibition of pentagastrin-stimulated gastric acid secretion by balloon distension of the antrum was unchanged by preceding intramuscular injection of metoclopramide. The inhibitory effect of antral distension on gastric acid secretion in healthy subjects does not seem to be mediated by secretin, cholecystokinin, bulbogastrone, neurotensin, or a dopaminergic mechanism.

Adult↗
PubMed1986

Inhibition of basal and betazole- and sham-feeding-induced acid secretion by omeprazole in man.

The effect of omeprazole, given as a buffered solution, on basal acid secretion and that induced by betazole and sham feeding in healthy subjects were studied. The three series of experiments showed a dose-dependent acid reduction during the 2nd to 4th h after administration of omeprazole in doses of 10-60 mg, with almost complete inhibition by the highest dose. The ED50 values were of the same magnitude for basal and stimulated acid secretion. This indicates that omeprazole is an equally potent inhibitor of both kinds of acid secretion irrespective of the manner in which the acid is activated.

Adult↗