[48-year-old patient with recurrent arthralgias and weight loss].
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Arthritis↗
Biomedical subjects
M V Singer
Publications and source records attributed to M V Singer.
Histamine H2 receptor antagonists and blood alcohol levels.
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Ethanol↗
Pancreatic and gastric responses to gastric versus jejunal beer in humans.
To investigate the influence of beer on gastric and pancreatic secretion, 14 fasted volunteers were studied on two different days. A multilumen intestinal tube allowed measurement of intraluminal pressures and collection of gastric and duodenal juices. Seven subjects received in random order 250 ml of either beer or glucose (5.6%, w/v) intragastrically; seven other subjects received these intrajejunally. After 15 min, 48 +/- 8% of beer and 47 +/- 6% of glucose were emptied into the duodenum. Intragastric beer induced a nearly sevenfold increase in gastric acid output as compared with glucose (16.3 +/- 2.9 mmol/h versus 2.5 +/- 0.6 mmol/h; p less than 0.05), intrajejunal beer induced a nearly threefold increase (5.1 +/- 0.8 mmol/h versus 1.7 +/- 0.3 mmol/h). The stimulated gastric acid output was threefold higher after intragastric than after intrajejunal beer. Trypsin output was slightly but significantly (p less than 0.05) stimulated by intragastric beer as compared with glucose (4,639 +/- 460 U/h versus 3,628 +/- 399 U/h) and nearly threefold by intrajejunal beer (2,579 +/- 455 U/h versus 849 +/- 181 U/h) (p less than 0.05). Trypsin response to intragastric beer was 1.8 times higher than after intrajejunal beer (p less than 0.05). Intragastric beer induced a nearly ninefold increase of the 1 h integrated plasma gastrin response as compared with glucose (998 +/- 347 pM min vs 115 +/- 70 pM min) (p less than 0.05). Intrajejunal beer and glucose did not release gastrin. We conclude that both intragastric and intrajejunal beer stimulate gastric acid and pancreatic enzyme secretion; intragastric beer being a more potent stimulant. Gastrin might partially mediate the responses to intragastric but not to intrajejunal beer.
Adult↗
Pancreatic bicarbonate response to HCl 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 pancreatic bicarbonate output and release of secretin in response to intraduodenal HCl before and after stepwise removal of the extrinsic nerves of the pancreas, i.e., celiac and superior mesenteric ganglionectomy alone or truncal vagotomy alone and truncal vagotomy plus celiac and superior mesenteric ganglionectomy. Ganglionectomy alone did not alter the incremental bicarbonate response to HCl. Truncal vagotomy alone significantly (P less than 0.05) decreased the incremental bicarbonate response to low (1.5 and 3 mmol/h) but not high (6 to 24 mmol/h) loads of HCl. Additional ganglionectomy restored the bicarbonate response to prevagotomy levels. With the extrinsic nerves intact and after ganglionectomy, but not after truncal vagotomy and truncal vagotomy plus ganglionectomy, intravenous atropine (14 nmol.kg-1.h-1) significantly reduced the incremental bicarbonate response to low (1.5 and 3 mmol/h) but not high loads of HCl. Neither the different surgical procedures nor atropine significantly altered plasma levels of secretin basally and in response to intestinal HCl. We conclude that 1) cholinergic fibers within the vagus nerves but not the splanchnic nerves are important mediators of the pancreatic bicarbonate response to low loads of HCl and 2) release of secretin by intestinal HCl is not under cholinergic and splanchnic control.
Animals↗
Nervous control of gastric and pancreatic secretory response to 2-deoxy-D-glucose in the dog.
The relative contribution of the vagus and splanchnic nerves as mediators of the action of 2-deoxy-D-glucose (2-DG) on the stomach and the pancreas is largely unknown. In conscious dogs with gastric and pancreatic fistulas, the effect of 2-DG (100 mg kg-1, given as an intravenous bolus) on gastric acid and pancreatic exocrine secretion was tested before and after bilateral truncal vagotomy and after truncal vagotomy plus celiac and superior mesenteric ganglionectomy (i.e. extrinsic denervation of the stomach and the pancreas). In another set of dogs, only ganglionectomy was performed and the same experiments were done as in the first set of dogs. With the extrinsic nerves intact, 2-DG caused a rapid (within 15 min) and prolonged increase in gastric acid output as well as in pancreatic flow rate, bicarbonate and protein output. Truncal vagotomy abolished the gastric acid and pancreatic secretory response to 2-DG; additional ganglionectomy had no further effect. Ganglionectomy alone did not significantly alter 2-DG-stimulated gastric acid output, pancreatic flow rate and bicarbonate output; protein output, however, was significantly diminished by 57%. These results indicate that (a) intravenous 2-DG is a potent stimulant of gastric acid and pancreatic bicarbonate and protein output; (b) the vagus nerves are the major mediators of the gastric and pancreatic secretory response to 2-DG; (c) the sympathetic nerve fibers running through the celiac and superior mesenteric ganglia are probably not involved in the mediation of the 2-DG-induced gastric acid and pancreatic bicarbonate secretion. The diminished protein response to 2-DG after ganglionectomy is probably due to cut vagal fibers running through these ganglia.
Animals↗
Alcohol and gastric acid secretion in humans: a short review.
The action of ethanol and alcoholic beverages on gastric acid secretion and release of gastrin in healthy, nonalcoholic humans is reviewed. Intravenous ethanol causes a dose-dependent stimulation of gastric acid output without releasing gastrin. The action of intragastric instillation of pure ethanol on gastric acid secretion is related to its concentration: concentrations of 1.4% and 4% (v/v) are moderate stimulants; concentrations of 5% to 40% (w/v) have no or rather an inhibitory effect. Oral, intragastric, and intraduodenal administrations of ethanol do not release gastrin, whereas beer and white and red wine but not whisky and cognac are potent stimulants of gastric acid secretion and release gastrin in humans. The stimulatory mechanism of low ethanol concentrations is unknown. Nonalcoholic constituents of beer and wine are most likely responsible for the strong stimulatory action of both beverages on gastric acid secretion and release of gastrin.
Alcoholic Beverages↗
[Singultus--causes and therapy].
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Hiccup↗
[Does a single oral dose of famotidine influence the blood alcohol level?].
Six healthy volunteer medical students (three men and three women) on four separate occasions drank 500 ml of beer or 250 ml of white wine 30 min after having taken 40 mg of famotidine or a placebo (after 48 hours of abstinence and six hours of fasting). Administration of drug or placebo followed a double-blind, randomized protocol. There was no demonstrable effect of famotidine on the serum level of alcohol (maximal values 0.29-0.67 mg/dl) or on the time until maximal serum concentrations of alcohol were reached.
Adult↗
[Inhibition of meal-stimulated secretion of gastric acid and liberation of gastrin by a new synthetic prostaglandin E2 derivative].
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Adult↗
[Clinicopathologic conference. Cholestasis syndrome in epithelioid cell granuloma of the liver: diagnostic and therapeutic difficulties].
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Adenocarcinoma, Scirrhous↗
Cholecystokinin-58 is the major circulating form of cholecystokinin in canine blood.
Cholecystokinin-58 (CCK-58) is the largest and most abundant, biologically active form of cholecystokinin in canine intestinal mucosa. Despite the high amounts in mucosa, CCK-58 has not been detected in significant amounts in the circulation. The release of CCK-58 into the peripheral blood in response to an intraduodenal perfusion of sodium oleate (9.0 mmol h-1) was studied in seven conscious dogs. Plasma (50 ml) was obtained before and after endogenous stimulation by a newly developed method that prevents in vitro degradation of large cholecystokinins. The relative abundance of immunoreactive forms of CCK was studied by high pressure liquid chromatography (HPLC) which separated the gastrin and CCK forms. Column eluates were measured with an antibody which recognizes the intact carboxyl terminus of both gastrin and CCK. Cholecystokinin immunoreactivity increased over basal in plasma by 7 fmol/ml after intraduodenal perfusion with sodium oleate. The most abundant form of stimulated cholecystokinin immunoreactivity eluted on HPLC in the position of CCK-58 (63% of total immunoreactivity found). Since CCK-58 is biologically active and is the most abundant circulating form, it should play an important role in the physiology of cholecystokinin.
Animals↗
Pancreatic polypeptide response to a meal before and after cutting the extrinsic nerves of the upper gastrointestinal tract and the pancreas in the dog.
The role of the sympathetic and parasympathetic innervation in the release of pancreatic polypeptide (PP) basally and in response to a meal was studied after stepwise extrinsic denervation of the pancreas and the upper gastrointestinal tract in conscious dogs with gastric fistulae. One set of seven dogs was fed a meat meal (35 g/kg body weight) before and after truncal vagotomy and after truncal vagotomy plus celiac and superior mesenteric ganglionectomy, ie, extrinsic denervation of the pancreas and the upper gastrointestinal tract. In another set of six dogs, only ganglionectomy was performed. Experiments were repeated in the presence of atropine (50 micrograms/kg body weight, given as an intravenous bolus 60 min prior to the meal). Truncal vagotomy significantly (P less than 0.05) reduced the postprandial 120-min integrated plasma PP response (IPPPR) by 84% as compared to the prevagotomy response. Before truncal vagotomy, atropine significantly reduced the IPPPR by 57%. After truncal vagotomy, atropine completely abolished the residual PP response. Additional celiac and superior mesenteric ganglionectomy did not alter the IPPPR already reduced by truncal vagotomy. With the vagus nerves intact, ganglionectomy alone had no effect on the IPPPR whether or not atropine was given. These findings indicate that (1) the splanchnic nerves do not play a significant role in postprandial PP release and (2) that the vagus nerves are important mediators of the response to a meal. The effect of atropine on postprandial PP release after truncal vagotomy may be due to interruption of short enteropancreatic reflexes, suppression of the intrinsic cholinergic activity of the pancreas, or inhibition of hormonally induced PP release.
Animals↗
Action of ethanol and some alcoholic beverages on gastric acid secretion and release of gastrin in humans.
The action of intragastric ethanol in various concentrations (1.4%-40% vol/vol) and of beer, white wine, cognac, and whisky on gastric acid secretion and release of gastrin was studied in healthy humans. Ethanol concentrations of 1.4% and 4% (vol/vol), but not higher, significantly (p less than 0.05) increased gastric acid secretion to 23% and 22%, respectively, of incremental maximal acid output [i.e., observed response to pentagastrin (6 micrograms/kg s.c.) minus basal acid output]. The 1-h incremental gastric acid responses to beer and wine were 96% and 61%, respectively, of incremental maximal acid output. Neither cognac nor whisky had any stimulatory effect. The 1-h incremental gastric acid response to an 8% peptone meal was 40% of incremental maximal acid output, and to peptone plus white wine 77%. Plasma gastrin levels were not altered by ethanol, cognac, and whisky. The 1-h integrated plasma gastrin responses to beer and white wine were 119% and 77%, respectively, of the response to the peptone meal. We conclude that (a) the action of pure ethanol on gastric acid secretion is related to its concentration: concentrations of 1.4% and 4% are moderate stimulants; concentrations of 5%-40% have no effect, or rather an inhibitory effect; (b) beer and white wine, but not whisky and cognac, are potent stimulants of gastric acid secretion; (c) the stimulatory mechanism of low ethanol concentrations is unknown; and (d) nonalcoholic constituents of beer and wine are most likely responsible for the stimulatory actions of both beverages on gastric acid secretion and release of gastrin.
Adult↗
A new round in the discussion on the action of secretin on pancreatic protein secretion: a further study on the effect of secretin on pancreatic secretion in dogs.
Whether or not secretin stimulates pancreatic protein secretion is a controversial question. In this investigation, dose-response studies with different secretin preparations were performed in dogs with two different types of pancreatic fistulae. Pure natural secretin (Karolinska Institute, Stockholm), synthetic secretin (Hoechst, Frankfurt), synthetic secretin (Hoechst, Frankfurt), synthetic D-Ala17-secretin (Roche, Basel), and natural secretin (Kabi, Munich) were tested in dogs equipped with a Thomas cannula for collection of pure pancreatic juice. The synthetic secretin was also tested in dogs with a modified Herrera fistula. Potency of the pure natural and the unmodified synthetic secretins was similar. Whereas protein output was significantly stimulated by these secretin preparations, protein concentrations fell to approximately 10 mg ml-1 with incremental doses of infused secretin. The high protein concentrations of 60 up to 120 mg ml-1 found in pure basal pancreatic secretion, suggest that pancreatic protein output may have been a "washout" phenomenon, and that the increasing protein output values were due to rising volume flow of pancreatic juice which is not completely protein-free. Impure secretin preparations and indirect collection techniques also lead to an elevation of pancreatic protein output.
Animals↗
Effect of rioprostil, a synthetic prostaglandin E1 on meal-stimulated gastric acid secretion and plasma gastrin levels in humans.
The effects of rioprostil (a newly developed synthetic prostaglandin E1 analogue) on meal-stimulated gastric acid secretion was evaluated in 8 healthy human volunteers. Gastric acid output was measured by intragastric titration on 4 different occasions. The following procedure was invariably employed: after a basal period of 45 min, 5 peptone meals (8%, 500 ml each) were given intragastrically in 45-min intervals and gastric acid output was measured continuously. 45 min after the first meal, either placebo or 150, 300 or 600 micrograms of rioprostil were given intragastrically in a randomized order and on different days. 15 min later, the second meal was given and intragastric titration continued. Rioprostil caused a dose-dependent inhibition of the 3-hour integrated gastric acid response to the peptone meals. The percentage of inhibition was 41, 68 and 79%, respectively, for 150, 300 and 600 micrograms of rioprostil. Whereas the inhibition by the two highest doses was statistically significant, this was not the case for the lowest dose of rioprostil. The integrated 3-hour plasma gastrin response to the peptone meals was not significantly changed by any of the doses of rioprostil. No significant adverse effects were observed with rioprostil.
Adolescent↗
Pancreatic secretory response to intestinal stimulants: a review.
In humans and many laboratory animals, protein digestion products such as peptides and amino acids and fat digestion products such as fatty acids and monoglycerides are potent intestinal stimulants of pancreatic enzyme secretion. The pancreatic enzyme response to these intestinal stimulants is related to the perfused load (amount per unit time) rather than to concentration. Both neural and hormonal pathways mediate the enzyme response to these intestinal stimulants. Enteropancreatic, cholinergic, vago-vagal reflexes are probably the most important mediators of the enzyme response to low loads of amino acids and fatty acids; hormones, such as cholecystokinin, seem to be the major mediators of the response to high loads of amino acids and fatty acids. Under physiological conditions it is probably the interplay of neural and hormonal mechanisms which regulates the pancreatic response to these stimulants. Gastric acid is the major regulator of postprandial pancreatic bicarbonate secretion. Secretion released by HCl is probably the most important physiological hormonal mediator of postprandial pancreatic bicarbonate secretion; its effect being potentiated by extrinsic (vagal) and intrinsic (intrapancreatic) cholinergic nerves and release of other hormones, such as cholecystokinin.
Amino Acids↗
[Neural control of pancreatic secretion].
In humans and many laboratory animals, protein and fat digestion products are potent intestinal stimulants of pancreatic enzyme secretion. Both neural and hormonal pathways mediate the enzyme response to these intestinal stimulants. Enteropancreatic, cholinergic, vago-vagal reflexes are probably the most important mediators of the enzyme response to low loads of amino acids, fatty acids and HCl; hormones, such as cholecystokinin, seem to be the major mediators of the response to high loads of amino acids, fatty acids and HCl. Gastric acid is the major regulator of postprandial pancreatic bicarbonate secretion. Secretin released by HCl is probably the most important physiological hormonal mediator of postprandial pancreatic bicarbonate secretion; its effect being potentiated by extrinsic (vagal) and intrinsic (intrapancreatic) cholinergic nerves and release of other hormones, such as cholecystokinin. Under physiological conditions it is probably the interplay of neural and hormonal mechanisms which regulates the pancreatic response to intestinal stimulants. However, this interaction of nerves and hormones is greatly unknown.
Amylases↗
[Regulation of gastric acid secretion: new aspects].
The purpose of this short review is to reveal new aspects of regulation of gastric acid secretion. The complex interactions between humoral, paracrine, neurocrine, neuroendocrine, vagal and sympathetic mechanisms will be emphasized. The finding that stimulation of the vagus nerves releases bombesin from peptidergic nerve fibers, which causes release of gastrin from endocrine cells in the stomach, demonstrates the complex interaction between nerves and hormones. The target organ, the parietal cell, has receptors for gastrin, acetylcholine and histamine, which potentiate each other regarding stimulation of acid secretion. New findings about the pathophysiology of acid secretion in duodenal ulcer patients are emphasized.
Animals↗