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M V Singer

Publications and source records attributed to M V Singer.

At least 163 records · Page 9Linked to original sources
PubMed1987

[Effect of circadian rhythm on gastrointestinal motility].

In western civilization, circadian rhythms of the gastrointestinal tract are dominated by a digestive-interdigestive rhythm: During the day interdigestive activity is rare because of frequent meal intakes prior to termination of preceding fed states: in contrast, nocturnal activity is largely interdigestive. Digestive and interdigestive functions are characterized by specific and interactive motor and secretory activity patterns. When exogenous influences via food intake are prevented, additional, underlying, endogenous, circadian rhythms are observed that modulate gastric and intestinal motility in a characteristic fashion, possibly with tight links to the central nervous system. It is likely that disturbances of physiologic circadian modulation of gastrointestinal function may have pathogenic importance.

Animals↗
PubMed1986

[Diagnostic significance of gastrointestinal hormones].

Determination of gastrointestinal hormones by radioimmunoassay in plasma is important for detection of endocrine-active tumours in the gut. Since in most cases multiple endocrine tumours occur, a variety of hormones such as gastrin, vasoactive intestinal polypeptide, glucagon, somatostatin, pancreatic polypeptide and neurotensin should be measured. Gastrin is helpful as a diagnostic tool in differentiating between Zollinger-Ellison syndrome and antral G-cell hyperplasia or hyperfunction. Autonomic neuropathy of the gut (as in diabetics) can be detected by measurements of plasma pancreatic polypeptide. The diagnostic value of measurements of plasma cholecystokinin, secretin and other gut peptide hormones is not yet defined.

Gastrins↗
PubMed1986

Effect of rabbit anti-pancreatic polypeptide serum on postprandial pancreatic exocrine secretion in dogs.

To determine whether pancreatic polypeptide (PP) is a physiologic inhibitor of pancreatic secretion, we have studied the effects of normal rabbit serum and anti-PP serum on pancreatic secretion during infusion of a physiologic dose of PP or intragastric food instillation in dogs. Infusion of 180 pmol/kg X h of PP, previously incubated with normal rabbit serum, induced increases in plasma PP (220 +/- 21 pmol/L) similar to those after the meal (213 +/- 51 pmol/L) and was accompanied by significant inhibition of pancreatic flow rate, bicarbonate output, and protein output (p less than 0.05) stimulated by secretin and cholecystokinin (n = 6). However, when the effect of exogenous PP was studied after in vivo administration of anti-PP serum or after previous in vitro incubation with anti-PP serum, no inhibition of pancreatic secretion was found, indicating that immunoneutralization of PP blocks the biologic activity of the hormone. Intragastric instillation of 400 ml of liver extract resulted in significant increases in pancreatic flow rate and outputs of protein and bicarbonate (p less than 0.01; n = 8), both during administration of normal rabbit serum and anti-PP serum. The postprandial increase in pancreatic secretion during administration of anti-PP serum was not significantly different from that during administration of normal rabbit serum. We, therefore, conclude that PP is not a physiologic inhibitor of postprandial pancreatic secretion.

Animals↗
PubMed1986

Action of atropine on the pancreatic secretory response to secretin before and after cutting the extrinsic nerves of the pancreas in dogs.

In two sets of dogs with gastric and pancreatic fistulas, we studied the effect of atropine on the pancreatic secretory response to intravenous secretin before and after cutting the extrinsic nerves of the pancreas, i.e., celiac and superior mesenteric ganglionectomy alone or truncal vagotomy plus celiac and superior mesenteric ganglionectomy. Neither truncal vagotomy alone nor ganglionectomy alone, nor the two together, altered the incremental bicarbonate response to secretin. Irrespective of the degree of integrity of the extrinsic vagal and splanchnic innervation of the pancreas, intravenous atropine (14 nmol/kg X h) significantly (p less than 0.05) depressed the incremental bicarbonate responses to the two lowest (5.2 and 10.3 pmol/kg X h) doses of secretin by 85% and 61%, respectively, but had no significant effect on responses to high doses. We conclude that the pancreatic bicarbonate response to secretin, and the action of atropine on that response, are independent of an intact extrinsic innervation of the gland. The observation of the persistent inhibitory action of atropine after extrinsic denervation of the pancreas is compatible with the hypothesis that endogenous cholinergic activity augments the pancreatic bicarbonate response to secretin.

Animals↗
PubMed1986

Action of intravenous ethanol and atropine on the secretion of gastric acid, pancreatic enzymes, and bile acids and the motility of the upper gastrointestinal tract in nonalcoholic humans.

To investigate the influence of the cholinergic nerves on the action of i.v. ethanol on interdigestive gastric acid, pancreatic enzyme, and bile acid output, seven healthy volunteers were studied. On each of 4 different days, they swallowed a multilumen intestinal tube system that allowed the measurement of intraluminal pressures and the collection of gastric and duodenal juice. The subjects received an i.v. infusion of either ethanol (600 mg/kg for 30 min followed by 3 mg/kg/min), atropine (5 mu/kg/h), a combination of both drugs, or NaCl. Whereas ethanol did not significantly influence motility, atropine induced motoric quiescence. Ethanol significantly (p less than 0.05) stimulated gastric acid output, by 55%, whereas atropine inhibited it by 91%. When ethanol and atropine were given together, gastric acid output was significantly higher than during atropine use alone. Both ethanol and atropine inhibited pancreatic amylase output--by 47% and by 82%, respectively. The degree of inhibition was 80% when ethanol and atropine were given simultaneously. Atropine but not ethanol significantly reduced bile acid output. The finding that atropine did not completely reverse the stimulating effect of i.v. ethanol on gastric acid secretion suggests that ethanol stimulates gastric acid secretion not only by a cholinergic but also by a noncholinergic mechanism. The observation that atropine did not reverse the inhibiting effect of ethanol suggests, but does not prove, that the effect of ethanol on the pancreas is predominantly mediated by cholinergic nerves.

Adult↗
PubMed1986

Dose-response effects of atropine on pancreatic secretory response to intravenous cerulein in dogs.

In conscious dogs with gastric and pancreatic fistulas, we studied the effect of i.v. atropine in doses ranging from 1.8 to 29 nmol/kg/h on the pancreatic secretory response to i.v. cerulein in doses ranging from 3.7 to 118 pmol/kg/h. Cerulein was given with an i.v. background infusion of secretin (20.5 pmol/kg/h), started 1 h before the lowest dose of cerulein was given. Secretin alone did not stimulate pancreatic protein output above basal. Doses of 7 and 29 nmol/kg/h of atropine significantly (p less than 0.05) decreased the protein output during secretin. A dose of 29 nmol/kg/h, but not lower doses, of atropine significantly inhibited the bicarbonate response to secretin. A dose of 3.7 pmol/kg/h and all higher doses of cerulein significantly stimulated bicarbonate and protein output above the value observed during secretin alone. None of the three doses of atropine given had any significant effect on the incremental bicarbonate and protein responses to cerulein. Secretin and cerulein did not alter basal heart rate; only the highest dose (29 nmol/kg/h) of atropine significantly increased heart rate. These findings are compatible with the hypothesis that cholinergic nerves do not alter the effect of exogenous cerulein, a CCK analogue, on pancreatic bicarbonate and protein secretion in dogs.

Animals↗
PubMed1986

Dose-response effects of atropine on pancreatic secretory response to intestinal tryptophan in dogs.

In dogs with gastric and pancreatic fistulas, we studied the effect of intravenous infusion of atropine in doses of 0.9, 1.8, 7, and 29 nmol X kg-1 X h-1 on the pancreatic secretory response to graded loads of intraduodenal infusions of tryptophan, given with a secretin background. Infusions of 1.8, 7, and 29, but not 0.9 nmol X kg-1 X h-1 of atropine sulfate significantly (P less than 0.05) decreased the incremental protein response to all loads of tryptophan. The cumulative incremental protein output was reduced by 44, 37, and 52%, respectively. Infusions of 1.8, 7, and 29 nmol X kg-1 X h-1 of atropine significantly decreased by approximately 50% the incremental bicarbonate response to low (0.12 and 0.37 mmol/h) but not high loads (1.1, 3.3, and 10 mmol/h) of tryptophan. The inhibitory potency of the effective doses of atropine did not differ significantly. Only the highest dose of atropine significantly increased heart rate by 76%. These findings indicate that 1) in the intact animal, the minimal dose of atropine required for inhibition of pancreatic bicarbonate and protein response to intraduodenal tryptophan seems to be 1.8 nmol X kg-1 X h-1, a dose that causes probably few systemic effects, since it does not increase heart rate; and 2) the inhibitory action of atropine on the pancreatic response to tryptophan appears to be an "all-or-none" effect.

Animals↗
PubMed1986

Action of intragastric ethanol on pancreatic exocrine secretion in relation to the interdigestive gastrointestinal motility in humans.

On different days, fasted volunteers were given either 100 ml of ethanol (40% v/v), glucose (isocaloric to ethanol) or distilled water intragastrically; the instillations always starting during the first observed duodenal phase I of the interdigestive migrating complex (IMC). Both ethanol and glucose produced a fed pattern of motility but only glucose significantly (P less than 0.05) delayed the reappearance of a new duodenal phase III of the IMC when compared to water. Ethanol and glucose significantly increased the 1-h duodenal bicarbonate output 7- and 16-fold, respectively. Glucose, but not ethanol, stimulated the duodenal amylase output when compared to water. Glucose, but not ethanol, caused a significant rise in plasma gastrin concentration; plasma secretin levels not being altered by both substances. We conclude that in non-alcoholic humans, an intragastric administration of ethanol in a concentration present in whisky and in an amount that is consumed in ordinary social drinking has a weak stimulatory action on pancreatic bicarbonate secretion and that this action is not mediated by release of secretin.

Adult↗
PubMed1985

[The pancreas and alcohol].

The action of acute and chronic administration of ethanol on pancreatic exocrine secretion in humans and several animal species is reviewed. If the data concerning the secretory action of ethanol on the pancreas are to the property assessed, several experimental variables have to be considered. Acute intravenous administration of ethanol inhibits basal and hormonally stimulated pancreatic secretion of bicarbonate and protein in nonalcoholic humans and most species of animals tested. Oral or intraduodenal ethanol causes moderate stimulation of pancreatic bicarbonate and enzyme secretion. Since anticholinergic agents and truncal vagotomy diminish the ethanol-induced inhibition of pancreatic secretion in the intact animal, it is possible that the action of ethanol on the pancreas is at least partly mediated by inhibitory cholinergic mechanisms. The action of ethanol on the pancreas may also be mediated by release of gastrointestinal hormones. Intravenous and oral administration of ethanol releases gastrin in dogs but not in humans. Pancreatic polypeptide is unlikely to be the hormonal mediator of the ethanol-induced inhibition of exocrine pancreatic secretion in humans and dogs, since ethanol does not release pancreatic polypeptide. The main secretory changes induced by chronic alcoholism in humans and dogs are increased basal secretion of pancreatic enzymes and decreased basal bicarbonate output, and these secretory changes may favour the occurrence of protein precipitates which are believed to be the first lesion of chronic pancreatitis in man. A decrease in the concentration of "pancreatic stone protein" in pancreatic juice may favour the development of protein precipitates in chronic alcoholic patients.

Acute Disease↗
PubMed1985

Gastrin response to a meal before and after cutting the extrinsic nerves of the stomach in the dog.

Atropine inhibits the post-prandial gastrin release after truncal vagotomy in the dog. Whether this action of atropine is due to suppression of stimulatory cholinergic fibres in the sympathetic nerves of the stomach and the upper small intestine or due to blockade of intrinsic gastric cholinergic mechanisms is unknown. Conscious dogs were fed a meat meal (35 g/kg body weight) before and after truncal vagotomy and after truncal vagotomy plus coeliac and superior mesenteric ganglionectomy. Experiments were repeated in the presence of atropine (50 micrograms/kg body weight, given as an i.v. bolus 60 min prior to the meal). In another set of dogs, only ganglionectomy was performed and the same experiments were done as in the first set of dogs. Truncal vagotomy enhanced the post-prandial 120 min integrated plasma gastrin response by 2.6 times as compared to the response with the vagus nerves intact. Before truncal vagotomy, atropine enhanced the integrated plasma gastrin response by 2.6 times; after truncal vagotomy atropine suppressed this response by 2.3 times. After truncal vagotomy, with or without atropine, additional coeliac and superior mesenteric ganglionectomy did not alter the integrated plasma gastrin response. With the vagus nerves intact, ganglionectomy alone had no effect on the integrated plasma gastrin response whether or not atropine was given. The finding that atropine suppresses the post-prandial plasma gastrin response to a meal after truncal vagotomy and coeliac and superior mesenteric ganglionectomy, i.e. cutting the extrinsic nerves of the stomach and the upper small intestine, suggests the existence of stimulatory cholinergic intrinsic fibres located within the stomach.

Animals↗
PubMed1985

Dose-response effects of atropine on pancreatic response to secretin before and after truncal vagotomy.

In dogs with gastric and pancreatic fistulas, we studied the effect of intravenous atropine in doses ranging from 0.9 to 58 nmol X kg-1 X h-1 on the pancreatic secretory response to secretin before and after truncal vagotomy. Truncal vagotomy did not alter the incremental bicarbonate response to secretin. Before and after truncal vagotomy, 7 nmol X kg-1 X h-1 and all higher doses of atropine sulfate significantly decreased the bicarbonate response to low doses (5.2 and 10.3 pmol X kg-1 X h-1) of secretin but had no significant effect on responses to high doses (20.5 and 41 pmol X kg-1 X h-1). The inhibitory potency of the effective doses of atropine did not differ significantly. Secretin did not stimulate pancreatic protein output above basal. Truncal vagotomy reduced protein output basally and during secretin by about 50%. Before and after truncal vagotomy, 7 nmol X kg-1 X h-1 and all higher doses of atropine significantly decreased protein output basally and during secretin. Secretin and truncal vagotomy did not alter basal heart rate. Only the three highest doses (14, 29, and 58 nmol X kg-1 X h-1) of atropine significantly increased heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Different actions of intravenous ethanol on basal (= interdigestive) secretion of gastric acid, pancreatic enzymes and bile acids and gastrointestinal motility in man.

The action of an intravenous infusion of ethanol (10% v/v; given in a dose of 300 mg kg-1 body weight for 30 min followed by 3 mg kg-1 min-1 for 2 hr) on the basal (= interdigestive) gastrointestinal motor activity and the basal gastric acid, pancreatic amylase and bile acid secretion was determined in 6 healthy human volunteers. Ethanol did not affect the duration of the interdigestive motor complex and the output of bile acids into the duodenum. Ethanol significantly (P less than 0.05) stimulated the gastric acid output by about 2.2-fold and inhibited the pancreatic amylase output by about 43% as compared to control experiments in which an intravenous infusion of 0.15 M NaCl was given. Ethanol did not alter the mean plasma levels of gastrin and pancreatic polypeptide as compared to prestimulatory values and to control experiments. In conclusion, these results show that intravenous ethanol given in a moderate dose stimulates gastric acid output and inhibits pancreatic amylase output in fasting non-alcoholic human beings. The mechanism(s) of these different actions of ethanol is unknown since release of gastrin or pancreatic polypeptide by ethanol does not account for the observed effects of intravenous ethanol.

Adult↗