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At least 937 records · Page 52Linked to original sources
PubMed2000

The effects of ammonia on pancreatic enzyme secretion in vivo and in vitro.

BACKGROUND: Recent studies clearly demonstrate that Helicobacter pylori (H. pylori) infection of the stomach causes persistent elevation of ammonia (NH3) in gastric juice leading to hypergastrinemia and enhanced pancreatic enzyme secretion. METHODS: The aim of this study is to evaluate the influence of NH4OH on plasma gastrin level and exocrine pancreatic secretion in vivo in conscious dogs equipped with chronic pancreatic fistulas and on secretory activity of in vitro isolated acini obtained from the rat pancreas by collagenase digestion. The effects of NH4OH on amylase release from pancreatic acini were compared with those produced by simple alkalization of these acini with NaOH. RESULTS: NH4OH given intraduodenally (i.d.) in increasing concentrations (0.5, 1.0, 2.0, 4.0, or 8.0 mM/L) resulted in an increase of pancreatic protein output, reaching respectively 9%, 10%, 19%, 16% and 17% of caerulein maximum in these animals and in a marked increase in plasma gastrin level. NH4OH (8 x 0 mM/L, i.d.) given during intravenous (i.v.) infusion of secretin (50 pmol/kg-h) and cholecystokinin (50 pmol/kg-h) reduced the HCO3 and protein outputs by 35% and 37% respectively, as compared to control obtained with infusion of secretin plus cholecystokinin alone. When pancreatic secretion was stimulated by ordinary feeding the same amount of NH4OH administered i.d. decreased the HCO3- and protein responses by 78% and 47% respectively, and had no significant effect on postprandial plasma gastrin. In isolated pancreatic acini, increasing concentrations of NH4OH (10(-7)-10(-4) M) produced a concentration-dependent stimulation of amylase release, reaching about 43% of caerulein-induced maximum. When various concentrations of NH4OH were added to submaximal concentration of caerulein (10(-12) M) or urecholine (10(-5) M), the enzyme secretion was reduced at a dose 10(-5) M of NH4OH by 38% or 40%, respectively. Simple alkalization with NaOH of the incubation medium up to pH 8.5 markedly stimulated basal amylase secretion from isolated pancreatic acini, whereas the secretory response of these acini to pancreatic secretagogues was significantly diminished by about 30%. LDH release into the incubation medium was not significantly changed in all tests indicating that NH4OH did not produce any apparent damage of pancreatic acini and this was confirmed by histological examination of these acini. CONCLUSIONS: 1. NH4OH affects basal and stimulated pancreatic secretion. 2. The excessive release of gastrin may be responsible for the stimulation of basal pancreatic enzyme secretion in conscious animals, and 3. The inhibitory effects of NH4OH on stimulated secretion might be mediated, at least in part, by its direct action on the isolated pancreatic acini possibly due to the alkalization of these acini.

Alkalies↗
PubMed1975

The effects of endotoxemia and bacteremia on gastrointestinal drug absorption in mice and rats.

Endotoxin [lipopolysaccharide (LPS)] from four Gram-negative bacteria injected i.v. delayed absorption of drugs administered in solution by gastric tube to mice and rats. Salicylate and guinine absorption was delayed at LPS doses from 50 to 400 mug/kg. Salicylate absorption was delayed by LPS when drug was given by gastric tube, while LPS did not affect drug levels when salicylate was given i.p. or intraduodenally. Bethanechol prevented the LPS effect and LPS pretreatment also protected against delayed absorption. LPS- treated rats retained more drugs in their stomachs after 30 minutes and their plasma salicylate levels were lowered. Everted intestinal sacs from LPS-treated rats transferred salicylate as well as controls. Thus, LPS delays gastrointestinal drug absorption solely by retarding gastric emptying. Escherichia coli urinary tract infection did not reproduce LPS delay of drug absorption, but the effects of systemic bacteria were similar to those of endotoxemia.

Animals↗
PubMed1975

Comparative effects of metoclopramide and bethanechol on lower esophageal sphincter pressure in reflux patients.

The effects of oral metoclopramide, 10 and 20 mg, bethanechol, 25 mg, and placebo on lower esophageal sphincter pressure (LESP) were studied in 15 men with symptoms of gastroesophageal reflux and basal LESP less than 11 mm Hg. Each drug produced a significant increase in LESP when compared to placebo. Metoclopramide, 20 mg, produced a greater increase than either metoclopramide, 10 mg, or bethanechol, 25 mg. Serum gastrin concentrations were not altered by any of the drugs. Side effects were unremarkable. The LESP increasing effect of metoclopramide might be useful in treatment of gastro-esophageal reflux.

Administration, Oral↗
PubMed1975

Effect of urecholine and carbacholine on pentagastrin-stimulated gastric secretion after proximal gastric vagotomy in duodenal ulcer patients;.

Six months after proximal gastric vagotomy gastric secretion was examined after infusion of pentagastrin, 15 mug/kg/hr, alone and in combination with urecholine, 60 mug/kg/hr, or carbacholine, 2 mug/kg/hr. There were no significant differences between mean acid outputs after the three types of stimulation. Pepsin outputs were significantly higher after pentagastrin plus carbacholine and pentagastrin plus urecholine than after pentagastrin alone. Urecholine and carbacholine increased pepsin secretion to a similar degree. Volume of gastric juice was significantly higher after simultaneous infusion of pentagastrin and urecholine than after pentagastrin alone or pentagastrin plus carbacholine.

Adult↗
PubMed1975

Inhibition of gastrin-stimulated canine acid secretion by sham-feeding.

In dogs with a Heidenhain pouch and oesophageal and gastric fistulae, sham feeding inhibited pentagastrin-stimulated Heidenhain pouch acid output. When secretion was stimulated with a combination of pentagastrin and betanechol chloride, the inhibitory effect of sham feeding was less pronounced. Histamine-stimulated secretion was not inhibited by sham feeding. The inhibitory effect was not affected by extragastric abdominal vagotomy but was reduced or abolished by truncal vagotomy. The results are consistent with the hypothesis that vagal activity releases a hormone which has an inhibitory action on gastric acid secretion.

Animals↗
PubMed1975

Urecholine test for denervated bladder-.

In the dog the denervation supersensitivity response of the detrusor appears within 7 to 21 days after bilateral pelvic nerve transection. Unilateral denervation cannot be detected by the standard Urecholine test.

Animals↗
PubMed1975

[Effects of cyclic AMP and urecholine on gastric secretion in the dog].

The influence of cyclic AMP on gastrin release from the canine antrum was investigated by a direct in vivo method. After removal of spleen, gastric corpus, pancreas and intestine an antral pouch was consecutively perfused with dibutyryl cyclic AMP, papaverin and bethanechol-HCl using a branch of the left gastroepiploic artery. A relevant rise of gastrin in portal blood was only observed during perfusion of bethanechol chloride. Thus cyclic AMP does not release gastrin from the canine antrum.

Adenosine Monophosphate↗
PubMed1976

The effects of cholinergic agents on ovarian contractility in the rabbit.

Cholinergic nerves have been recognized in the ovaries of several species. Smooth muscle fibers have also been demonstrated within the ovary, and it has been suggested that these elements are involved in the ovulatory process. Ovarian contractility was investigated in 49 ovaries from 25 rabbits in in vivo and in vitro systems and correlated with the time of hCG-induced ovulation. Effects of 6 cholinergic drugs on ovarian contractility were recorded at various intervals from 6 to 20 hours after administration of hCG. Cholinergic agents were administered via the abdominal aorta in the in vivo preparations and added to the bath for in vitro studies. In general, acetylcholine, bethanechol and pilocarpine exerted variable effects. Atropine depressed ovarian contractile activity. No definitive pattern of altered sensitivity to cholinergic drugs could be identified as the time of ovulation was approached; however, a relationship was observed between the amount of cholinergic drug administered and effects on ovarian contractions.

Acetylcholine↗
PubMed1976

Effect of growth hormone release-inhibiting hormone on gastric secretion, mucosal blood flow, and serum gastrin.

In dogs with gastric fistulae and Heidenhain pouches (HP) growth hormone release-inhibiting hormone (GH-RIH) infused intravenously in a dose of 2.5 mug per kg per hr inhibited almost completely acid and pepsin responses to pentagastrin, Urecholine, and a peptone. Histamine-induced acid secretion was more resistant to the inhibition by GH-RIH, and only acid secretion evoked by the lower doses of histamine was suppressed by this peptide. The inhibition of pentagastrin-induced gastric secretion was associated with a marked reduction in mucosal blood flow. The ratio of aminopyrine concentration in the gastric juice and blood plasma was not significantly changed by GH-RIH, indicating that the reduction in mucosal blood flow was secondary to an inhibition of gastric secretion. Gastric acid and serum gastrin responses to a peptone meal adjusted to pH 5.0 and kept in the main stomach at this same pH by intragastric titration were significantly decreased by GH-RIH, indicating that the observed acid inhibition could be attributed at least in part to the suppression of gastrin release. GH-RIH inhibited acid secretion from HP stimulated by liver extract in HP. The finding that GH-RIH inhibits gastric secretion induced by exogenous stimulants as well as by the direct chemical stimulation of the HP mucosa without changing serum gastrin level suggests that the major action of GH-RIH is a direct suppression of the oxyntic glands.

Animals↗
PubMed1976

Return of esophageal peristalsis in idiopathic achalasia.

A 47-year-old male was diagnosed as having idiopathic achalasia on the basis of clinical, roentgenographic, and manometric criteria. He was on no medication and had no disorders known to impair esophageal motility. He was treated by pneumatic dilation with a good clinical response. On reexamination 7 years later, several features considered to be typical of achalasia were no longer present. Changes included return of peristaltic activity throughout most of the body of the esophagus, failure of a direct-acting cholinergic agent to produce an increase in base line intraesophageal pressure, and failure of a direct-acting cholinergic agent to produce a heightened response at the lower esophageal sphincter (LES). Incomplete LES relaxation in response to swallowing persisted. This represents the first reported case of return of esophageal peristalsis in idiopathic achalasia.

Bethanechol Compounds↗
PubMed1976

Studies on the mechanism of esophagitis-induced lower esophageal sphincter hypotension in cats.

Perfusion of 0.1 n HC1 5 cm above the lower esophageal sphincter (LES) in cats for 30 min on 4 consecutive days produced biopsy-documented esophagitis and marked decreases in LES pressure. Using this model the effects of experimental esophagitis on the LES response to edrophonium, pentagastrin, and bethanechol were determined. The sphincter response to both edrophonium and pentagastrin after esophagitis was induced was significantly less than preperfusion responses. When the esophagitis had resolved, the pressure response to edrophonium and pentagastrin returned to preperfusion levels. In contrast, the sphincter response to bethanechol during esophagitis was not different from the preperfusion response and remained unchanged after resolution of the esophagitis. Lower esophageal smooth muscle taken from cats with active esophagitis appeared normal by both light and electron microscopy. These studies indicate that besides decreasing resting LES tone, esophageal inflammation causes functional impairment of a cholinergic mechanism regulating LES pressure. In contrast, the smooth muscle appears to be unaffected by inflammation despite the LES hypotension.

Animals↗
PubMed1976

Genesis of basal sphincter pressure: effect of tetrodotoxin on lower esophageal sphincter pressure in opossum in vivo.

Currently it is believed that lower esophageal sphincter closure is maintained by tonic neurohormonal activity. Studies were performed to evaluate the role of neural and myogenic activity in the genesis of resting sphincter pressure in the opossum. The neural activity in the sphincter was blocked by intravenous administration of the puffer fish poison, tetrodotoxin, in intact animals. The respiration in these animals was assisted with a respirator, their blood pressure was supported by intravenous administration of Ringer's solution, and their body temperature was maintained by heating lamp. The lower esophageal sphincter pressures were measured with water-filled and continuously perfused catheters which were anchored to the lower esophageal sphincter using a new technique. Tetrodotoxin blocked the sphincter response to neural stimulation with vagal stimulation, esophageal distention, and local electrical stimulation of the sphincter. The mean resting sphincter pressure before tetrodotoxin was 59.0 +/- 2.6 mm Hg, and it was 64.4 +/- 6.9 mm Hg after tetrodotoxin (P greater than 0.05). During neural block with tetrodotoxin, the sphincter response to administration of isoproterenol or bethanechol was similar to that during the control period (P greater than 0.05). These studies show that: (1) Tetrodotoxin can be administered in intact animals to achieve complete block of neural activity in the lower esophageal sphincter; (2) sphincter muscle is not adversely affected by tetrodotoxin; and (3) block of neural activity does not alter the resting lower esophageal sphincter pressure.

Animals↗