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PubMed1987

Intraluminal release of serotonin, substance P, and gastrin in the canine small intestine.

Several gastrointestinal hormones have been found in the intestinal lumen, but as yet their physiologic role is not yet clear. We have previously shown in anesthesized animals that electrical vagal stimulation provokes simultaneous intraluminal release of serotonin (5-HT) and substance P (SP). The aim of this study was to investigate if a physiologic stimulus, a meal, releases 5-HT, SP, and gastrin (G) into the canine jejunum. In 10 dogs, chronic jejunal Thiry-Vella loops were perfused with saline (37 degrees C) before and after: a test meal; atropine, 0.2 mg/kg intravenously before the meal; atropine alone at the same dose; propanolol, 0.5 mg/kg intravenously before the meal; and propanolol alone at the same dose. Effluent perfusates and peripheral blood samples were assayed by radioimmunoassay for concentrations of 5-HT, SP, and G. Large amounts of all three humoral agents were found intraluminally during the interdigestive period. The meal resulted in increased circulating levels of 5-HT, SP, and G, while intraluminal concentrations of 5-HT and SP but not G increased following the meal. Both atropine and propanolol pretreatment significantly reduced this response, while alone, these drugs did not affect basal values. We postulate that 5-HT and SP released into the intestinal lumen in response to a meal act as local neurocrine/paracrine modulators. Their release mechanisms appear to be under both cholinergic and adrenergic control.

Animals↗
PubMed1992

Effect of meal composition and sham feeding on duodenojejunal motility in humans.

The disruptive effect of meals of different fat content and caloric value and of sham feeding on the interdigestive migrating motor complex (IDMMC) was studied in eight healthy subjects using an ambulatory recording system that allowed continuous monitoring of small bowel motility for three consecutive days. The durations of fed pattern were not significantly different between meals of 800 kcal/50% fat, 400 kcal/50% fat, and 800 kcal/25% fat, but were significantly longer compared to IDMMC cycle length and sham feeding. The latter two were not significantly different. On a separate day, five subjects consumed a meal of 400 kcal/9% fat and a second one of 800 kcal/50% fat. The duration of the fed pattern following the high fat meal was significantly longer than the low fat one. Sham feeding significantly increased plasma concentrations of gastrin and neurotensin (NT), but did not affect those of cholecystokinin (CCK), insulin, and peptide YY (PYY). The various variables of the IDMMC were not different during the two nights of the study, and velocity of migration of phase III during the first day and both nights was similar. We conclude that the duration of the fed pattern depends, in part, on the composition of the meal. Sham feeding, resulting in an increase in both plasma gastrin and NT concentrations, does not disrupt the IDMMC. When using thin probes, IDMMC is stable during prolonged recording.

Adult↗
PubMed1981

Insulin and myoelectric activity of the small intestine of the pig.

The effect of insulin on the myoelectric activity of the small intestine was determined in conscious pigs. Animals were implanted with electrodes along the small intestine, a strain gage on the stomach and catheters in both saphenous arteries. Feeding modified the migrating myoelectric complex (MMC), a cyclic pattern of action potential activity of the small intestine characteristic of fasting. The first period of regular spiking activity (RSA) on the duodenum after feeding was delayed and was not followed by quiescence. Plasma insulin and glucose concentrations during the first three MMC after feeding were highest just before periods of duodenal RSA. Injection or infusion of insulin into fasted pigs with production of hypoglycemia caused disruption of stomach motility and duodenal electrical activity. The duodenal MMC was not altered when glucose to prevent hypoglycemia was infused together with insulin or when glucose was infused alone. These studies suggest that insulin is not directly responsible for the postprandial modification of MMC activity as insulin infusions only modify the MMC when hypoglycemia occurs.

Action Potentials↗
PubMed1981

Pancreatic exocrine secretion and immunoreactive secretin release after intraduodenal instillation of 1-phenyl-1-hydroxy-n-pentane and HCl in rats.

Portal plasma immunoreactive secretin (IRS) concentrations, pancreatic juice flow, and amylase output were simultaneously measured in response to intraduodenal infusion of 1-phenyl-1-hydroxy-n-pentane (PHP), as well as infusion of hydrochloric acid (HCl). These data were compared with those obtained from intravenous bolus injections of synthetic porcine secretin in anesthetized rats. The intraduodenal infusion of PHP or HCl at a rate of 2 ml/min for 2 min produced a dose-related increase in portal plasma secretin concentrations, pancreatic juice flow, and amylase output. However, the mechanism of secretin release by PHP seems to differ from that of HCl. The secretin response to 0.1 N HCl infused at a rate of 0.1 ml/min for 30 min was complete after 10 min, despite continued infusion, while PHP stimulated a secretin release which persisted for 10 min after cessation of infusion. The pH in the second portion of the duodenum, following PHP infusion, remained consistently greater than 6.3. PHP-stimulated pancreatic exocrine secretions were only partially suppressed by somatostatin, while secretin release was almost completely inhibited. However, intraduodenal PHP may stimulate the release of secretin along with other gastrointestinal hormones, and the endogenous release of these hormones may not be inhibited by somatostatin.

Amylases↗
PubMed1986

Overview of misoprostol clinical experience.

Misoprostol is an E1 prostaglandin analog. Most of the other synthetic prostaglandins that are being studied in advanced clinical trials for gastrointestinal diseases are E2 derivatives. Misoprostol has shown a dose-related antisecretory effect that lasted 3-5.5 hr. In addition, animal studies have shown cytoprotective properties that are being confirmed in clinical studies. Ulcer-healing trials using four times daily dosing appear to parallel the antisecretory dose-response curve up to a dose of 200 micrograms qid. Evidence presented in this supplement suggests a further increase in healing-rate response at 300 micrograms misoprostol qid. The misoprostol healing rates obtained in duodenal ulcer and gastric ulcer therapy at 200 micrograms qid are not significantly different from those seen in the same studies with cimetidine at a dose of 300 mg qid. No significant rebound in recurrence has been observed during follow-up for 12 months after short-term 100- and 200-micrograms qid misoprostol treatment. The most frequent adverse effects are dose-related diarrhea and abdominal cramping, which are transient in most patients and have not caused a significant problem in clinical use. There is also a tropic effect on the pregnant uterus, which was observed in a special pharmacologic clinical study. No significant abnormalities have been detected in clinical laboratory tests or gastric biopsies. There have also been no adverse effects noted on blood pressure, pulse, platelets, the immune system, pulmonary function, gastrointestinal hormones, or the endocrine system. These previously discussed characteristics of misoprostol, and current data, suggest that this prostaglandin E1 derivative may be an important addition to the treatment of peptic ulcer disease.

Alprostadil↗
PubMed1979

Does motilin regulate canine interdigestive gastric motility?

Our objective was to determine whether motilin increases the frequency of cyclic interdigestive motor activity in the canine proximal stomach. In 4 conscious dogs with autotransplanted proximal gastric pouches and gastrointestinal electrodes, intravenous infusions of motilin (0.6 microgram/kg body wt/hr) increased the frequency of the interdigestive cycles by 30% both in the pouch and in the main gastrointestinal tract. However, the 3-min interval between the end of a cycle in the pouch and the end of a cycle in the duodenum was unchanged by motilin. In control experiments, without motilin infusion, the concentration of endogenous motilin in the plasma during the intense contractile phase of the cycles (overall mean 385 pg/ml) was greater in each dog (P less than 0.01) than the concentration during the quiescent phase (overall mean, 256 pg/ml). The concentration of plasma motilin was also greater in the contractile phase (mean, 717 pg/ml) than in the quiescent phase (mean, 587 pg/ml) during exogenous infusions of motilin in two of three dogs (P less than 0.01). We concluded that motilin increased the frequency of cyclic interdigestive motor activity in the canine proximal stomach and that the increase was not dependent on intact proximal gastric extrinsic innervation.

Action Potentials↗
PubMed1983

Interdigestive motilin secretion and gallstone disease.

Plasma motilin concentrations were measured in eight controls and 11 patients with radiolucent gallstones over a period of 3-4 h following an overnight fast. In five of these patients the interdigestive motor complex (IDMC) was studied simultaneously. The results indicate: a) cyclical changes of plasma motilin concentrations (mean cycle duration 110 +/- 9.9 and 102 +/- 8.4 min, means +/- SEM) and a significant correlation between the basal intercyclical motilin concentrations and the age (p less than 0.02) in the controls and the gallstone patients studied, and b) a significant correlation between the maximal motilin increase and the age in the controls (p less than 0.01) but not in the gallstone patients. The results therefore suggest a different behaviour of the interdigestive motilin patterns in controls and gallstone patients. As the motilin cycles were accompanied in 90% with an IDMC in the five patients studied this conclusion might include an abnormal interdigestive motor activity within the intestinal tract in gallstone patients.

Cholelithiasis↗
PubMed1990

GR 38032F (ondansetron), a selective 5HT3 receptor antagonist, slows colonic transit in healthy man.

The newly recognized class of 5-hydroxytryptamine receptors (5HT3) may be involved in the induction of nausea, since their pharmacological antagonists are effective against emesis induced by chemotherapy. 5HT3 receptors are present on enteric neurons, and 5HT3 blockers may produce mild constipation; we thus hypothesized that 5HT3 receptors would modulate colonic motility. To determine if GR 38032F, a selective 5HT3 antagonist known to have antiemetic effects, influences colonic transit in health, a randomized, double-blind, placebo-controlled crossover study was performed. Using a radiopaque marker technique, colonic transit was quantified in 39 healthy volunteers (19 men, 20 nonpregnant women) 18-70 years of age. On a standard 25-g fiber diet, 16 mg of GR 38032F was given orally thrice daily. Gastrointestinal peptides (peptide YY, human pancreatic polypeptide, neurotensin, motilin, gastrin-cholecystokinin, substance P) were also measured in plasma fasting and postprandially. Mean total colonic transit time on placebo was 27.8 hr, while on GR 38032F it was 39.1 hr (P less than 0.0005). Transit times through the left colon (P less than 0.0005) and rectosigmoid (P less than 0.05) were prolonged by the drug, but right colonic transit was not significantly altered. Transit times did not correlate with age or gender, but subjects with shorter transit times were significantly more affected than were those with longer transit times. The peak release of peptide YY was minimally decreased following GR 38032F (P less than 0.01), but the peak and integrated postprandial responses of human pancreatic polypeptide, neurotensin, motilin, gastrin-cholecystokinin, and substance P were not significantly altered by the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1989

Bombesin: an activator of specific Aeromonas antibody secretion in rat intestine.

The effect of bombesin (BBS) in modulating the secretion of specific Aeromonas antibodies in rat intestine was determined. Rats were immunized with the culture supernatant of Aeromonas hydrophila, isolate SSU. This culture supernatant contained a number of toxins that may be considered virulence factors. After 24 days of immunization, rats were anesthetized and a 10-cm intestinal segment was perfused with phosphate-buffered saline. The effluents were collected for measurement of IgA and IgG by the enzyme-linked immunosorbent assay. When compared with the effect of intravenous administration of normal saline in the control group, intravenous injection of BBS (20 micrograms/kg) in the experimental group caused a significant increase in rat intestinal IgA and IgG in perfusates. The stimulatory effects of BBS on the presence of IgA and IgG were depressed partially by proglumide, a receptor antagonist of cholecystokinin (CCK) and gastrin. Treatment with pentagastrin (250 micrograms/kg) accelerated intestinal secretion of IgA, but failed to stimulate intestinal IgG secretion. In addition, intravenous injection of CCK-8 (120 ng/kg) evoked the intestinal secretion of either IgA or IgG. These findings demonstrated that BBS, gastrin, and CCK can stimulate antibody secretion in rat intestine and the stimulatory effect of BBS may be mediated partially via release of CCK and gastrin. These results suggest that neuropeptides such as BBS and gastrointestinal hormones, eg, CCK and gastrin, may participate in the regulation of intestinal secretion of IgA and IgG antibodies, respectively, in rats.

Aeromonas↗
PubMed1979

Endocrinology of duodenal ulcer.

Several gastrointestinal peptides with proven or suggested endocrine or paracrine functions influence gastric acid secretion, gastrointestinal motility, and mucosal blood flow. Increased or decreased release of such factors could participate in the pathogenesis of duodenal ulcer disease by inducing increased gastric acid concentration in the duodenal bulb. To date, increased stimulation of parietal cells by gastrin has been demonstrated only in patients with gastrinoma, G-cell hyperplasia, gastric outlet obstruction, hyperparathyroidism, excluded antrum, and short bowel syndrome, but not in the usual duodenal ulcer disease. Also, a defective inhibition of parietal cell function by endocrine or paracrine factors, such as gastric inhibitory polypeptide, secretin, somatostatin and vasoactive intestinal polypeptide, seems not to exist in patients with duodenal ulcer disease. However, as long as the physiology of gastrointestinal peptides in gastric secretion and motility is not understood, a possible role of these factors in the pathogenesis of simple duodenal ulcer disease cannot be excluded.

Duodenal Neoplasms↗
PubMed1977

Effect of synthetic motilin on gastric motor activity in conscious dogs.

The effect of intravenous infusion of synthetic motilin on gastric motor activity was investigated by means of chronically implanted force transducers in 4 conscious dogs. Since the gastric motor pattern consisted of two major subpatterns, digestive and interdigestive motor activity, motilin was tested for its motor stimulating activity in both states. It was found that motilin had no influence upon gastric motor activity in the digestive state. However, during the interdigestive state, intravenous infusion of motilin in doses of 0.3-2.7 microgram/kg/hr induced motor activity similar to the naturally occurring interdigestive contractions in a dose-related fashion. Since motilin is released by duodenal alkalinization in the dog, it may be postulated that motilin is a substance to control the interdigestive contractions in the dog, although other reports describe motilin release by duodenal acidification and inhibition of gastric emptying in man. Endogenous stimuli leading to motilin release may be different among species. The present study clearly indicates that motilin induces a contractile pattern similar to that seen during the interdigestive state in conscious dogs.

Animals↗
PubMed1993

Autonomic dysfunction in patients with chronic intestinal pseudo-obstruction.

We prospectively evaluated autonomic function in 50 patients with clinical and manometric features of a neuropathic form of chronic intestinal pseudo-obstruction (CIP). In 26 patients, there were underlying disease processes that may have affected extrinsic neural control to viscera: diabetes mellitus (n = 16), previous gastric surgery (n = 5), and other neurologic disorders (n = 5). Our aim was to characterize autonomic function in these patients, and those 24 with CIP unassociated with a known underlying neurologic disorder (idiopathic group). We assessed vagal function and sympathetic cholinergic and adrenergic function by means of standardized autonomic tests and quantitated postprandial antral pressure activity. We also measured postprandial levels of pancreatic polypeptide and neurotensin as indicators of vagal function and of the delivery of nutrients to the distal small bowel. Among the idiopathic group (n = 24), two had evidence of a generalized sympathetic neuropathy and five abdominal vagal dysfunction (one had both). Among diabetic patients, three had sympathetic adrenergic failure, six had orthostasis with normal plasma noradrenaline, ten had signs of generalized sympathetic neuropathy and eight had abdominal vagal dysfunction. Vagal dysfunction was identified in all three patients who underwent vagotomy as part of their previous gastric surgery. In the other neurologic syndromes, vagal function was abnormal in three of the five patients. Thus, autonomic and, particularly, vagal dysfunction are confirmed in a majority of patients with CIP associated with known diabetes or neurologic disorders; however, a previously unrecognized autonomic (chiefly vagal) neuropathy of undetermined cause has been identified in five of the 24 'idiopathic' CIP patients.

Autonomic Nervous System Diseases↗
PubMed1994

Cholecystokinin is not a major regulator in the digestive system in the chicken.

To find out whether physiological concentrations of cholecystokinin (CCK), a gastrointestinal hormone in mammals, are also active in chickens, the pancreatic amylase secretory response to CCK-8 was investigated in vitro. Rat pancreatic acini responded to the physiological concentration of CCK-8, but in chickens amylase release was induced at a concentration of CCK-8 1000 times higher than that observed in rats. In another experiment, biliary flow was tested with several doses of CCK-8. The bile flow was stimulated in a dose-dependent fashion, but a significant enhancement was not obtained at a concentration of 0.5 micrograms CCK-8/kg body weight, which was considerably higher than physiological ones. It is concluded that endogenous CCK does not have an important role in the digestive system in the chicken.

Amylases↗
PubMed1985

Neurotensin-like immunoreactivity in some preparations of secretin and cholecystokinin.

Commercially available cholecystokinin (CCK) from the Boots Company, Nottingham and to a lesser degree CCK from the Gastrointestinal Hormone Research Unit of Karolinska Institute Stockholm and from Kabi Diagnostica, Studsvik, and also secretin from the Boots Company have been found to contain neurotensin-like immunoreactive contamination. As neurotensin is able to stimulate pancreatic secretion, this admixture may be of relevance when pancreatic function is tested.

Cholecystokinin↗
PubMed1977

[Coffee and health].

Coffee as a rule develops stimulating effects on the central nervous system, heart and circulation which are mainly caused by caffeine. In certain cases coffee may also have a sedative effect and sometimes even it is useful to fall asleep quickly. Furthermore coffee may be advantageous in the treatment of some functional disorders caused by lacking of dopamine, because coffee is able to increase the dopamine formation in brain. Concerning the effects of coffee in the gastrointestinal-tract and liver-bile system caffeine is only of secondary importance. Hereby certain roasting substances, possibly also chlorogenic acid or caffeic acid should be responsible for the stimulating effects observed in these organs. These stimulating effects could be caused whether directly or indirect e.g. by liberating gastrin or other gastrointestinal hormones. Vitamin niacin, which is formed in greater amounts from trigonelline during the roasting process, may also be important from the nutritional standpoint. Therefore coffee may be prescribed as a true drug in cases of deficiency in vitamin niacin or also in the pellagra disease. By extensive epidemiological studies performed lately it could be demonstrated that there exists no correlation between coffee consumption and certain risk factors as hypertension, heart infarction, diabetes, gout or cancer diseases. Furthermore there was no evidence that coffee or its caffeine content are able to induce genetic alterations or even malformations.

Animals↗
PubMed1994

Effect of ileal oleate on interdigestive intestinal motility of the dog.

To determine the effect of ileal oleate on fasting intestinal motility, pairs of duodenal and ileal catheters and bipolar duodenal and jejunal seromuscular electrodes were surgically implanted in six dogs. The ileum was perfused with either normal saline (154 mM NaCl) or oleic acid emulsion (152 mM), while intestinal myoelectric activity was continuously monitored. For transit studies, a bolus of [3H]PEG was injected into the duodenum, and jejunal and ileal alliquots were collected every 15 min for a 6-hr study period. Plasma samples were collected for radioimmunoassays of peptide YY and enteroglucagon. Ileal oleate infusion increased the MMC cycle length and decreased the number of MMCs (P < 0.001) and the myoelectric spike-burst frequency/10 min in the duodenum (P < 0.05). Both duodenal-jejunal (P < 0.05) and duodenal-ileal transit (P < 0.01) were delayed markedly by ileal perfusion with oleic acid emulsion as compared to control studies. Ileal oleate increased plasma levels of peptide YY (P < 0.01) and enteroglucagon (P < 0.01). Ileal perfusion with oleate therefore activated the so-called "ileal brake," diminishing duodenal myoelectric spike bursts and slowing intestinal transit while concurrently increasing plasma levels of peptide YY and enteroglucagon.

Animals↗