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To assess the effects of endogenous GRP on vagal gastrin release and acid secretion, anti-GRP gamma-globulin was infused in anesthetized rats to bind endogenously released GRP. Anti-GRP gamma-globulin blocked the gastrin-releasing effects caused by 4 μg/kg/hr of exogenous GRP infusion and suppressed gastrin release by electrical vagal stimulation. In spite of this suppression, anti-GRP gamma-globulin did not alter basal or vagal-stimulated acid secretion. [ABSTRACT FROM AUTHOR]

The effects of gastrin releasing peptide (GRP) on gastrin release and gastric secretion were studied in anesthetized rats. Intravenous infusion of GRP (1-16 μg/kg/hr) caused a dose-dependent increase in serum gastrin level, however, it had no effect on basal gastric secretion in the lumen-perfused stomach preparation. Furthermore, GRP inhibited gastric secretion stimulated by pentagastrin or histamine dosedependently, but not by carbachol. Simultaneous infusion of GRP and a beta adrenergic blocking agent, propranolol, an inhibitor of somatostatin release, did not alter the inhibitory effect of GRP on pentagas trin-stimulated gastric secretion. These results suggest that the inhibitory effect of GRP on gastric secretion in a stimulated condition is mediated via peptide hormones coreleased by GRP, and not via betaadrenergic pathways. [ABSTRACT FROM AUTHOR]

The phospholipid content of basal and pentagastrin-stimulated gastric secretion was measured in 9 healthy volunteers. One week oral administration of teprenone did not alter the gastric acid and pepsin secretion. The phospholipid content was increased by teprenone. Changes in subclasses of phospholipids in gastric mucus by teprenone treatment, namely, increased phosphatidylcholine and decreased lysophosphatidylcholine, were observed. [ABSTRACT FROM AUTHOR]

In order to examine the role of vasoactive intestinal polypeptide (VIP) in systemic blood pressure and pancreatic and gastric secretions in rats, the peptide was given to rats either intravenously (i.v.) through the femoral vein or intracerebroventricularly (i.c.v.) through the lateral ventricle. VIP, when given i.V., showed a systemic, hypotensive effect and a stimulatory effect on pancreatic secretion in urethane-anesthetized rats. When VIP was given i.c.v., there was no change in systemic blood pressure and pancreatic secretion in urethane-anesthetized rats, nor in gastric secretion both in urethane-anesthetized, stomach-perfused rats and in conscious, chronic gastric fistula rats. More research is needed to determine the central effect of VIP in digestive secretion. [ABSTRACT FROM AUTHOR]

A method of establishing chronic gastric fistulae in rats is described. In rats with chronic gastric fistulae, the basal acid output was 48.8 ± 2.9 μEq/100 g/hr and the basal pepsin output was 543 ± 28 μg tyrosine/100 g/hr. The effects of urethane-induced anesthesia, pyloric ligation, and acute laparotomy on gastric secretion in rats were examined. Both urethane-induced anesthesia and acute laparotomy depressed gastric secretions. In Ghosh-Schild rats, the basal acid output was 3.2 ± 0.4 μEq/100 g/hr and the basal pepsin output was 70 ± 13 μg tyrosine/100 g/hr. The persistant and very low level of gastric secretion in these animals appears to result from the combination of both urethane anesthesia and invasive surgery. Because the rats with chronic gastric fistulae do not require anesthesia, invasive surgery, or pyloric ligation, which may play very important roles in the regulation of gastric functions, this kind of preparation is a suitable method for studying the physiology and pharmacology of gastric secretions in the rat. [ABSTRACT FROM AUTHOR]

Gastric acid and pepsin secretions were measured in antrum and fundus separately by perfusing each region of the stomach in anaesthetized rats. Perfusion of the antral region with alkaline and acid solutions did not affect gastric acid and pepsin secretions in the fundic gland region. Gastric secretions in the antrum and acid secretions in the fundus remained unchanged when each region of the stomach was instillated with glycine. Pepsin stimulation was observed in the fundic region only when perfused with glycine. We confirmed our previous observation that topical amino acid in the oxyntic gland stimulated pepsin secretion directly. The pepsin stimulatory effect of amino acid was found to be independent of antral regulation. [ABSTRACT FROM AUTHOR]

This study was undertaken to compare the potency of each L-and D-isomers of 5 amino acids in stimulating gastric acid and pepsin secretion by the intragastric reperfusion preparation in rats. Gastric basal and glycine-stimulated secretions in this preparation were lower than those Ghosh-Lai preparation, but not to a statistically significant extent. All D-and L-isomers of amino acids tested were found to markedly stimulate pepsin secretion, but to only slightly stimulate acid secretion. Pepsin stimulatory response to each D-and L-isomer of amino acid was similar. The stimulatory effects of amino acids thus seem to be unrelated to the optical stereoisomeric configuration. [ABSTRACT FROM AUTHOR]

Inhibitory effects of gastric inhibitory polypeptide (GIP) on tetragastrin-stimulated gastric acid secretion were studied in five dogs prepared with both Heidenhain fundic pouches and simple gastric fistulae. In the first series of experiments graded doses of GIP, doubling from 0.25 to 2.ug/kg-hr, were given intravenously with a background infusion of 4.0 ug/kg-hr tetragastrin. In the second experiments graded doses of tetragastrin, doubling from 1.0 to 8.0 ug/kg-hr, were given intravenously with an additional infusion of 0.5 ug/kghr of GIP. GIP inhibited dose-dependently gastric acid secretion from Heidenhain pouches, but not from simple fistulae. Lineweaver-Burk and Dowd-Riggs transformations of dose-response data obtained with tetragastrin alone and tetragastrin plus GIP showed similar D50 (the dose required for half-maximal response). This indicates that GIP acts as a noncompetitive inhibitor of tetragastrin on acid secretion from the denervated stomach. GIP, however, had no inhibitory effects on acid secretion from the innervated stomach. The cause of this paradoxical effect of GIP remains unknown. [ABSTRACT FROM AUTHOR]

Measurements of serum epinephrine and gastrin, simultaneously, gastric mucosal blood flow and gastric secretion were carried out in cinchophen treated dogs. No significant changes in either serum concentrations of epinephrine and gastrin or fundic mucosal microcirculation after a single 100mg/kg cinchophen administration were found while gastric secretion increased markedly after the medication. On the other hand, a significant increase in serum epinephrine and gastrin levels was observed while gastric secretion decreased significantly after large doses of cinchophen (300mg/kg) were injected intravenously. Here gastric mucosal microcirculation is decreased. Repeated administration of 100mg/kg cinchophen for 3 to 7 days brought about an increase in epinephrine and gastrin levels and caused an occurrence of fundic mucosal hemorrhage. Sympathetic discharge and gastrin release were not seen after a 3-week period of cinchophen administration. Cinchophen ulcers were produced, even when contact between the bile and the stomach mucosa was avoided. Vagotomy had no connection with ulceration and gastric secretion. [ABSTRACT FROM AUTHOR]

Gastric acid and pepsin secretions were measured in the perfusing rat stomach preparation with sodiumcitrate phosphate buffer, pH 6.6. In anesthetized rat stomach preparation, acid output in both basal and stimulated conditions seemed to be small, but pepsin output was observed even in a short period. In the rats which were fed freely just before use, basal pepsin output was significantly lower than that of fasted rats, although in the basal acid output and in the acid and pepsin output during stimulation in both groups, there was no difference statistically. Intravenous infusion of tetragastrin (1, 2, 4, 8, 16 and 32µg/kg/hr) produced a dose dependent acid and pepsin secretions. Tetragastrin, at the dose of 8μg/kg/hr, stimulated acid and pepsin output. Acid output was kept constant for three hours, but pepsin output was made to peak within an hour and formed a plateau after 1.5 hours at a level of 30% of peak pepsin output. [ABSTRACT FROM AUTHOR]

This experimental study was designed to determine the effects of different doses of prostaglandin E on gastric acid secretory function and ulceration in rats. Ulceration was induced by the method of Shay on 81 rats and by the method of stress on 114 rats. Ninety-seven rats were included in the experimental group, 98 rats constituted the control one. It has been established that three subcutaneous injection of prostaglandin E at the single dose of 540 μg per kg of body weight were found to have a marked inhibitory effect of this drug on the gastric juice volume, titration activity of free hydrochloric acid and total acidity. Distinct protective effects of this drug on the course of experimental ulcer were detected as well. Similar subcutaneous injections of prostaglandin E at the single dose of 180 μg per kg had no apparent inhibitory effect on the parameters mentioned. The studies of prostaglandin E action at the doses of 360, 1080 and 1800 μg per kg on ulceration induced by the combination of stress and intraperitoneal injections of histamine (at the dose of 7.5 mg/kg of body weight) were carried out. The results of these investigation showed the subcutaneous injections of Pg E at the dose of 1800 µg per kg to have a protective effect on the gastric mucosa. The data obtained give ground to suggest Pg E to be one of the factors in the protection of the gastric mucosa against ulcerogenic lesions due to the ligation of the pylorus and stress. [ABSTRACT FROM AUTHOR]

Intraduodenal instillation of hypertonic glucose significantly inhibited tetragastrin-induced gastric acid and pepsin outputs in man. The secretory volume of gastric juice was markedly decreased, whereas, acid concentration remained unchanged. Pepsin concentration, on the contrary, was reduced significantly. The degree of inhibition of pepsin output, therefore, was greater than that of acid output. No significant difference in the extent of inhibition of acid or pepsin output was observed between control subjects and patients with duodenal ulcer. [ABSTRACT FROM AUTHOR]

The gastric acid output was studied in the 11 patients of hyperparathyroidism before and after parathyroidectomy. The gastric acid output before operation was almost equal to the normal control in our hospital. After the correction of serum calcium by parathyroidectomy, the gastric acid output and serum gastrin were decreased. The decreased gastric acid output was recovered as the days passed since operation and approached to the preoperative level. The acid output in hyperparathyroidism was less in the case whose activity of alkaline phosphatase was more, which suggested that the calcium deposition on gastric mucosa might damage the parietal cell as the result of long lasting hypercalcemia. [ABSTRACT FROM AUTHOR]

An intraventricular administration of sulpiride suppressed the experimental cinchophen ulcer, thereby the effect of repeated administration of the material on cinchophen ulcerogenesis is evident, whereas intermittent administration lacked this effect. Such an effect as reducing experimental cinchophen ulceration, which is due to central neurohumoral mechanism, following intraventricular infusion of sulpiride appears to be ascribable to a chemical blockage of the hypothalamic structure. It can thus be concluded that sulpiride acts principally at the level of hypothalamus. Its inhibitory action on cinchophen gastric ulcer development is probably exerted via the hypothalomo-pituitary-adrenal axis, which is essential to the occurrence of an ulcer, and may be regarded as favoring the central neurohumoral theory of cinchophen ulcerogenesis. [ABSTRACT FROM AUTHOR]

The results reported here have compelling implications concerning gastric mucosal damage in detecting the mechanism of cinchophen-induced gastric lesions in dogs. The acute type of cinchophen gastric lesion, a condition characterized by bleeding and/or diffuse superficial gastric erosions of the fundic gland area, is indicative of so called 'stress ulceration' and may be due to activating intramucosal pepsinogen during a rapid increase in endogenous corticosteroid levels. Exogenously administered large doses of corticosteroid or cinchophen solely explained the existence of the correlation between gastric mucosajuice pepsin ratio (MJPR) and the gastric lesion. The greater the increase in MJPR, the greater the change in fundic glandular mucosal destruction. Thus the diffuse superficial mucosal destruction of the fundic gland area, occurring shortly after the medications, was estimated as intramucosal digestion. On the other hand, the chronic cinchophen ulcer in the antral mucosa would be due to both an increased output of gastric pepsin secretion and a decreased mucous secretion which is caused by continuous relatively high basal levels of the steroids. The importance of the role of corticoids in relation to gastric pepsin secretion was sufficiently estimated from the results of MJPR measurements. These findings provide information on the pathogenesis of two types of cinchophen induced gastric lesions. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Using gastrin-like AOC-tetrapeptide the secretory function of the stomach of Japanese with endoscopically normal gastric mucosa was examined in a multicenter clinical study. Mean one hour secretion volume, mean maximal acidity, and mean maximal acid output were found to be 129.3 ±60.0 ml/hr, 103.7 ±32. 4 mEq/1, and 9.2 ±6.9 mEq/hr respectively. Results were analysed according to sex or age by analysis of variance and compared further with the corresponding data reported in the literature. [ABSTRACT FROM AUTHOR]

The incidence of parietal cell antibodies (P.C.A.) in patients with various diseases was investigated by complement fixation test (C.F.T.). The relationship between the incidence of P.C.A. and clinical and pathological findings was also investigated. The incidence of P.C.A. with simple atrophic gastritis was 34.8% in total cases, 29.0% in male and 48.1% in female, respectively. The difference between the sexes was statistically significant (p<0.05). The incidence of P.C.A. in superficial gastritis was 37.5%, showing the same incidence as atrophic gastritis. The difference between the two groups was not statistically significant (p<0.05). The incidence in patients with hypo and hyperacidity was 43.0% and 11.8%, respectively. The difference was statistically significant, but that between hypo and normoacidity was not significant (p<0.05). The author postulated the conclusion that the superficial gastritis could be included in the category of atrophie gastritis. The dissociation of correlation of titer of C.F.T. with acidity and histological findings was found. The correlation was more significantly observed with acidity than with histological findings. The relatively high incidences of P.C.A. were noted in patients with peptic ulcer, gastric carcinoma and chronic thyroiditis. The incidence of P.C.A. in other diseases showed the nearly equal incidence to that of other investigators. Three cases of postgastrectomy patients were noted, in which the P.C.A. disappeared four to six months after total or subtotal gastrectomy. [ABSTRACT FROM AUTHOR]

To study the intestinal phase of ulcer inhibition, olive oil or hydrochloric acid was infused into small intestine in white male rats weighing 200-250 gr. The animals were fasted before study. Tetragastrin was administered continuously through the tail vein using the infusion pump. The ulcer formation by gastrin at the rate of 60% was decreased by the oil or hydrochloric acid infused into small intestine as well as by secretin administered intravenously (8 U/kg-h). The acid output and the rate of secretory volume were also inhibited by oil, HCl and secretin. Peptic output by gastrin was decreased by infusing the hydrochloric acid into small intestine, however olive oil in small intestine neither decreased nor augmented the peptic putout. Through these results the important role of small intestine in the inhibitory system of ulcerogenesis became obvious. To make clear the hyperacidity as one of the ethiological factors of peptic ulcer, the intestinal phase of gastric acid secretion should be investigated especially by the study of gastrointestinal hormone. [ABSTRACT FROM AUTHOR]

The pharmacological study of menatetrenone(2-methyl-3-all-trans-tetraprenyl-1,4-naphtoquinone) indicated that this compound inhibited experimental starvation and stress ulcers in the rats. It was also found effective on accelerating the healing process of experimental acetic acid ulcer and pylorus ligation ulcer. In the experimental ulcer of rats caused by serotonin, there showed non-significance in inhibition. The inhibitory pattern on every experimental condition, there showed markedly reduction of hemorrhagic tendency on the ulcerative area, and is capable of healing or preventing various types of experimental peptic lesions. On the other hand, it had no neuro-vegitative action and did not modify gastric secretion. From which it is concluded that, it has a vitamin-like mode of action and is a potent hemostatic. The application of this trans-type vitamin K-2 into a clinical therapeutic level of acute aggressive phase of peptic ulcer disease is strongly recommended. [ABSTRACT FROM AUTHOR]

The mechanism of the gastric antisecretory action of the stimulation of central alpha-2 adrenoceptors were studied in conscious, pylorus-ligated rats using intracerebroventricularly (i.c.v.) administered oxymetazoline as the model substance. I.c.v. administration of 10 μg of oxymetazoline strongly inhibited the secretion of acid, pepsin and fluid, whereas upon s.c. injection this dose was without any effect. Pretreatment with idazoxan abolished the antisecretory effect of i.c.v. administered oxymetazoline. I.c.v. injected oxymetazoline inhibited gastric secretion induced by carbachol in vagotomized rats, but the inhibitory effect was less pronounced than on the spontaneous secretion in rats with intact vagi. Hypophysectomy abolished the antisecretory effect of i.c.v. oxymetazoline, and pretreatment with the vasopressin antagonist, d(CH)Tyr(Me)AVP, significantly attenuated it. The results suggest that the inhibition of gastric secretion by the stimulation of central alpha-2 adrenoceptors in rats is mediated in part by vasopressin released from the pituitary gland. [ABSTRACT FROM AUTHOR]

Several α-adrenoceptor agonists given intracerebroventricularly or subcutaneously to rats were assessed for their effects on gastric secretion under condition of pylorus ligation. Intracerebroventricular injection of α-adrenoceptor agonists reduced gastric secretion, in the following order (relative potency, clonidine = 1): oxymetazoline (100) > clonidine (1) > methoxamine (0.024) > phenylephrine (0.003). The antisecretory effects of oxymetazoline and clonidine given intracerebroventricularly were antagonized with yohimbine administered by the same route. Subcutaneous injection of α-adrenoceptor agonists also reduced gastric secretion, in the following order (relative potency, clonidine = 1): clonidine (1) > oxymetazoline (0.3) ≫ phenylephrine (0.001) ∼ methoxamine (0.0006). Oxymetazoline, when given intracerebroventricularly, was most effective in decreasing the volume and titratable acidity of gastric secretion. Pretreatment with 6-hydroxydopamine intracerebroventricularly (250 μg/rat × 2; 72 and 120 h before) reduced the antisecretory effect of clonidine given intracerebroventricularly. Thus, gastric secretion appears to be regulated in an inhibitory manner by α-, but not by α- in the central and peripheral nervous systems, in pylorus-ligated rats. [ABSTRACT FROM AUTHOR]

An aspect of the vasomotor effect of nitrites and nitrates was studied by investigating the influence of these substances on the mucosal blood flow and hence on gastric secretion in the rat. Firstly, point measurements were obtained using an aminopyrine clearance technique after intravenous nitrite and nitrate treatment. Then with an appreciably different technique (C-aniline clearance on perfused stomach) the kinetics of the phenomenon were followed after, firstly, intravenous administration of the two agents and secondly their intragastric administration. It is interesting to note that nitrites and nitrates are active to differing degrees and present opposing effects: nitrites decrease whereas nitrates globally enhance the factors under consideration (gastric mucosal blood flow, gastric juice volume, acid and pepsin output). The strong action of nitrites, even though retarded, persists throughout intragastric perfusion. However, intravenously administered, nitrates have a more transitory effect and cause no modification on intragastric administration. The flow rate-gastric parameter correlations are significant in all cases and show modifications of the aqueous compartments of the body. [ABSTRACT FROM AUTHOR]

The effect of the phosphodiesterase inhibitor 4-(3-cyclopentyloxy-4-methoxyphenyl)-2-pyrrolidone (ZK 62711) on gastric secretion and the cyclic AMP system of the gastric mucosa was studied in rats and guinea pigs. In rats, 0.03-0.3 μmoles/kg ZK 62711 i.v. stimulated acid and pepsin secretion in a dose-dependent manner and 0.03 μmoles/kg i.v. enhanced the effect of histamine. In guinea pigs no reproducible stimulation was found after intravenous injections of ZK 62711. The stimulation of gastric secretion in the rat by 0.3 μmoles/kg ZK 62711 i.v. was not affected by vagotomy but was totally inhibited by 10 μmoles/kg cimetidine i.v. The structurally related phosphodiesterase inhibitor, 4-(3-butoxy-4-methoxybenzyl)-2-imidazolidine (Ro 20-1724), at the dose of 3.3 μmoles/kg i.v. stimulated gastric secretion in anaesthetised rats to a similar extent as 0.3 μmoles/kg ZK 62711 i.v. The content of cyclic AMP in the rat gastric mucosa in vivo was slightly increased by 10 μmoles/kg ZK 62711 i.v, whereas lower doses did not change it. Accumulation of cyclic AMP in the rat gastric mucosa by 50 μmoles/kg histamine i.v. was enhanced by simultaneous injections of 3.3 μmoles/kg ZK 62711 i.v. In rat gastric tissue slices in vitro 1-50 μM ZK 62711 increased the level of cyclic AMP but 100 μM histamine had no effect in the absence or presence of ZK 62711. In gastric mucosal slices of the guinea pig 10 and 50 μM ZK 62711 increased the cyclic AMP content which effect was inhibited by 100 μM cimetidine and enhanced the stimulatory effect of 100 μM histamine on cyclic AMP. The activity of soluble cyclic AMP phosphodiesterase was inhibited by ZK 62711 in the rat (IC=18 μM) and guinea pig gastric mucosa (IC=1.5 μM). Adenylate cyclase was not affected in the homogenate of the guinea pig gastric mucosa. The results indicate that the phosphodiesterase inhibitor ZK 62711 which increases cyclic AMP levels in the gastric mucosa in vivo and in vitro, is a potent stimulator of gastric acid secretion. [ABSTRACT FROM AUTHOR]

Acute gastric mucosal lesions are often observed after the intravenous administration of high doses of anticancer drugs. To investigate the acute toxic effects of such anticancer therapy on the gastric mucosa, 5-fluorouracil (5-FU) was administered intravenously to anesthetized rats. Gastric mucosal blood flow (GMBF) was measured continuously using laser Doppler velocimetry. Acid secretion was measured using a perfusion method for 1h after the administration of 5-FU. No significant change was observed with a low dose of 5-FU (50 mg/kg), but a high doses of 5-FU (100 or 200 mg/kg) caused a significant decrease in GMBF in a dose-dependent manner. The selective antagonist of the muscarinic acetylcholine receptor, pirenzepine, prevented the decrease in GMBF with high doses of 5-FU. Acid secretion decreased after the administration of 5-FU, but not significantly. This study indicates that a decrease in GMBF may be an important factor in gastric mucosal injury induced by chemotherapy. Pirenzepine may prevent the gastric mucosal lesions which are induced by the administration of 5-FU. [ABSTRACT FROM AUTHOR]

The effects of various synthetic benzimidazole derivatives on gastric H/K ATPase activity in vitro were examined. The results showed that the effects of substituents on the benzimidazole ring were not significant. However, replacement of sulfoxide connecting two ring systems to sulfide resulted in a completely inactive compound in vitro, suggesting the essential role of sulfoxide group in the inhibition. In addition, compounds with 5 or 6-membered oxacyclic substituents attached to the pyridine ring displayed the most effective inhibitory activity. Among these derivatives, AU-47 was the most potent, and detailed mechanistic studies with the compound were carried out. AU-47 inhibited gastric H/K ATPase in a concentration and time dependent manner with 50% inhibition at 6 μM. The presence of sulfhydryl reducing agents or substrate analogue protected H/K ATPase from the inactivation. The inhibition by AU-47 was potentiated by acid pretreatment of the compound, suggesting the structural conversion of AU-47 into a more active intermediate which was favored in acidic condition. Consistent with in vitro results, AU-47 inhibited in vivo gastric acid secretion. The results suggest that AU-47 is a relevant candidate for the development of new antiulcer agent. [ABSTRACT FROM AUTHOR]

An intravenous infusion of a 3% solution of amino acids was given to 8 dogs, all with Heidenhain pouches and gastric fistulae. Four of these had duodenal cannulae opposite the pancreatic and 4 opposite the biliary ampulla. The usual basal 100 min spontaneous peaking of pancreatic juice volume and protein secretion was seen but peaks were abolished by the amino acid infusion and troughs were slightly elevated, but the total 90 min volume protein and bicarbonate outputs were not different from control. Gastric acid and pepsin secretions were augmented reaching a peak during the first hour with a subsequent decline. The 90 min acid and pepsin output was significantly higher than control. The gallbladder contracted during the first hour and remained thus until the infusion was terminated. This happened even when the duodenum was kept alkaline, but was abolished by ganglionic blockade. During intravenous amino acid infusion the patterns of gallbladder activity and pancreatic secretion resembled those of the post cibal rather than fasting state. [ABSTRACT FROM AUTHOR]

Gastrin release and gastric secretion in response to i.v. dimethylxanthine (2 mg/kg for 5 min followed by a 55-min infusion of 2.5 mg/kg) were studied in 25 normal subjects. Gastrin release was significantly stimulated, whereas gastric acid and pepsin secretion was inhibited. The adenylcyclase activation may, therefore, play a role in the mechanism of gastrin release. Moreover, dimethylxanthine seems to be a useful aid in studies on G-cell function in man. [ABSTRACT FROM AUTHOR]

Skin resistance, sweat-gland counts, salivary flow, gastric secretion, and pH were measured in volunteers and patients of both sexes, Negroes and Caucasians. Correlational analysis suggested two negatively related clusters: (A) salivary flow, sweat-gland counts, and gastric secretion; and (B) age, skin resistance, and pH. Skin resistance was higher in Negroes than Caucasians, and in females than males. increasing irregularlv with age. [ABSTRACT FROM AUTHOR]

A new method has been devised for the collection of gastric secretion in conscious rats. A stainless steel wire loop was placed around the pylorus. Seven to 10 days later when the rat had recovered from the operation and was showing significant weight gains and food intake, it was starved for 48 h and collection of gastric juice was begun by tightening the wire loop. This effectively occluded the pylorus, and had the advantage that the animal remained conscious during the procedure. The rat was sacrificed after a certain period of time, and the gastric content was collected. After centrifugation, the total acidity of the supernatant was determined by titration with 0.01 N NaOH. With the present method, the total acid output as well as the rate of gastric secretion were significantly higher than those of similarly operated rats under restraint and those which were investigated using the Shay method. The gastric mucosa of each rat was examined and it was found that the incidence of gastric lesions in the control group using the present method was significantly lower than that in the other operated groups. This method is regarded as less unphysiological than the widely used Shay technique, in which pyloric ligation is performed in the unconscious rat immediately before the collection of gastric juice. [ABSTRACT FROM AUTHOR]

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In the presence of theophylline (10 M), histamine stimulated the production of cAMP by minced gastric tissue of guinea pigs in a dose-dependent manner. This stimulation was competitively inhibited by the histamine-receptor blocking agent burimamide but not by the histamine-receptor blocking agent diphenhydramine. Since the histamine-stimulated secretion of acid by the stomach is also inhibited by blockade of H-receptors but not by blockade of H-receptors, our findings support the role of cAMP as the mediator in the action of histamine on the secretion of gastric acid.-The antihypertensive drug clonidine increased the secretion of gastric acid in apparently the same way as histamine did, i.e. by stimulation of H-receptors and subsequent increase in the formation of cAMP. [ABSTRACT FROM AUTHOR]

The effect of phloxin (Na salt of tetrabromo-tetrachlorofluorescein) on histamine- and bethanechol-stimulated gastric acid secretion was studied in anaesthetized rats. Concentrations of phloxin, equimolar with those of the stimulants, depressed the secretory response to histamine and had no influence on the bethanechol effect. The results suggest that histamine is not involved in the events triggered by bethanechol which stimulate gastric acid secretion in rats. [ABSTRACT FROM AUTHOR]

1. The effect of 'antigastrin' (SC-15 396) on gastric acid and pepsin secretion produced by the gastrin-analogue tetrapeptide amide Try. Met. Asp. Phe-NH and by electrical stimulation of the vagus was investigated in anaesthetized gastric fistula cats. 2. 'Antigastrin' failed to inhibit both acid and pepsin response stimulated by either the tetrapeptide or vagus excitation. 3. It was concluded that the ineffectiveness of 'antigastrin' in cats is due to a species difference between rats and dogs on the one hand and cats on the other, and that 'antigastrin' is not a specific gastrin antagonist. [ABSTRACT FROM AUTHOR]

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In conscious dogs with Thiry-Vella loops of duodenum and Heidenhain pouches, gastric acid secretion stimulated by gastrin pentapeptide was depressed by fat emulsion or N/10 HCl in the loop. In contrast, when intravenous methacholine was the acid stimulus, both acid and fat in the loop increased secretion. Both these changes in acid secretion were abolished by local anesthetization of the loop mucosa. Since injected cholecystokinin-pancreozymin preparations depress gastrin pentapeptide stimulated acid secretion and augment methacholine stimulated secretion, it is concluded that in our experiments the mediator of the observed alterations in gastric acid secretion could be cholecystokinin-pancreozymin liberated by the fat emulsion and acid from the loop mucosa. [ABSTRACT FROM AUTHOR]

The effect of intravenous administration of commercially available Boot's secretin upon gastric secretion was studied in the pylorus ligated rat. Secretin had no effect on basal gastric secretion, nor on insulin and high dosage histamine stimulated gastric secretion. Secretin, however, showed a significant effect upon gastrin-like tetrapeptide stimulated gastric secretion. The inhibitory effect of secretin on gastrin stimulation appeared not only to lower gastric secretion stimulated by gastrin but also tended to depress the gastrin stimulated gastric secretion to below a basal level. This inhibitory effect against gastrin affected both the parameters of secretory volume and total acid output of gastric juice secreted from the pylorus ligated rat. It is concluded that, gastrin provides to gastric oxyntic cell the secretory stimulation for hydrochloric acid production as well as for a specific activating factor to activate secretin. This activated secretin plays a role in the inhibition of gastric secretion via the gastrin mechanism. [ABSTRACT FROM AUTHOR]

Effects of acetylcholine, tetra-gastrin, secretin, and CCK/PZ on gastric acid secretion, and blood sugar, plasma insulin (IRI) and plasma gastrin level were investigated in rats with induced duodenal fistula. In addition, interactions between these agents on acid secretion were also investigated in rats and partly in man. [ABSTRACT FROM AUTHOR]

Changes of plasma gastrin level following acetylcholine stimulation were determined using two-antibody technique in rat with and without atropine pre-treatment, and the results were compared with fluctuations of the gastric acid secretion and the ultrastructural findings of the antral G cell, simultaneously. Relations among these thus confirmed biochemically and electromicroscopically were discussed. [ABSTRACT FROM AUTHOR]