Revised classification of pancreatitis. Report of the Second International Symposium on the Classification of Pancreatitis in Marseille, France, March 28-30, 1984.
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Acute Disease↗
Biomedical subjects
M V Singer
Publications and source records attributed to M V Singer.
Action of ethanol on gastrin release in the dog.
In conscious dogs with gastric and duodenal Thomas fistulas, we studied the effect of ethanol on plasma concentrations of gastrin. Ethanol was given either as an infusion into a peripheral vein (1.95 M, 200 ml/hr) or into the duodenum (0.95 M, 400 ml/hr) or as an intragastric bolus injection. The effect of the intragastric bolus injection of 200 ml of different concentrations (0.3 M, 1.7 M, 6.85 M) of ethanol was compared with that of equimolar solutions of urea and sucrose (0.3 M, 1.56 M), and with that of sodium taurocholate (0.06 M) and distilled water. The gastrin responses to an oral mixed-meat meal (35 g/kg) were also investigated. Intragastric bolus injection of isoosmolar (0.3 M) ethanol, but not of equimolar solutions of urea and sucrose or H2O, significantly (P less than 0.05) increased plasma gastrin levels above basal. Hyperosmolar solutions of ethanol, urea, and sucrose as well as hypoosmolar sodium taurocholate produced a pronounced increase of plasma gastrin concentrations above basal. The comparison of the mean 2-hr integrated plasma gastrin responses (IRG) showed that ethanol (6.85 M), urea (6.85 M), and sodium taurocholate (0.06 M) are at least as potent stimuli of release of gastrin as the test meal used. Intraduodenal and intravenous infusion of ethanol did not significantly alter mean plasma gastrin concentrations. We conclude that in the dog ethanol, but not urea and sucrose, given in a concentration (0.3 M) which is known not to disrupt the gastric mucosal barrier, increases plasma gastrin levels.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Interdigestive gastrointestinal motility and secretion of gastric acid and pancreatic enzymes in young cigarette smokers.
The basal (interdigestive) gastrointestinal motor activity and the interdigestive gastric acid and pancreatic amylase secretion were determined in 10 young smokers (mean age 23 years) and 7 nonsmokers (mean age 26 years). There was no significant difference in the length of the interdigestive motor complex between smokers and nonsmokers, but the speed of transmission of the activity front (phase III) in the upper intestine was significantly (p less than 0.05) greater in smokers than in nonsmokers. No significant overall changes in the interdigestive gastric acid and pancreatic amylase outputs were observed between the two groups studied.
Adult↗
[Pancreatic polypeptide--an indicator of vagal tonus in the gastrointestinal tract and pancreas?].
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Digestive System↗
Pancreatic polypeptide response to ethanol in humans and dogs.
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Adult↗
Latency of pancreatic fluid secretory response to intestinal stimulants in the dog.
The effect of atropine and truncal vagotomy on the latency of the secretory response of the exocrine pancreas to rapid intraduodenal injection of L-tryptophan, sodium oleate and HCl or to rapid intraportal injection of secretin or CCK octapeptide has been determined in conscious dogs with pancreatic fistulae. The intraduodenal stimulants were injected either alone or in the presence of an intravenous infusion of secretin, CCK octapeptide or a combination of both hormones. The mean latency of response to tryptophan alone (62 +/- 2 s), oleate alone (64 +/- 5 s) and HCl alone (91 +/- 3 s) was significantly longer (P less than 0.05) than the latency to intraportal secretin (28 +/- 5 s) or CCK octapeptide (45 +/- 4 s). Infusion of secretin alone or with CCK octapeptide significantly shortened the latency of response to tryptophan (38 +/- 3 s) and oleate (41 +/- 5 s), but had no effect on the latency to intraduodenal HCl (96 +/- 4 s). Atropine and truncal vagotomy both increased the latency to intraduodenal tryptophan and oleate threefold but did not affect the latency to intraduodenal HCl or intraportal secretin or CCK octapeptide. These data support the hypothesis that the stimulus to pancreatic fluid secretion evoked by intraduodenal HCl is humoral rather than neural, while the responses to intraduodenal tryptophan and oleate are mediated, at least in part, via an enteropancreatic, vago-vagal, cholinergic reflex.
Animals↗
Beer and wine but not whisky and pure ethanol do stimulate release of gastrin in humans.
In humans, the action of ethanol on gastrin release is still unclear and that of alcoholic beverages greatly unknown. We studied the effect of a drink of various concentrations of pure ethanol and several commonly ingested alcoholic beverages on plasma levels of immunoreactive gastrin in 6 healthy human volunteers and compared the results to a protein-rich meal. A drink of distilled water (250 ml) and of pure ethanol (250 ml or 125 ml in the case of 40% v/v ethanol) in concentrations (4, 10, 20 and 40% v/v) normally present in beer, wine, liquor and whisky did not stimulate plasma gastrin levels above basal. Of the alcoholic beverages given only whisky (125 ml) did not stimulate gastrin release. Beer, red and white wine (250 ml each) caused a rapid increase in plasma gastrin concentrations with a peak at 15-20 min, basal levels being reached 60 min after starting the drink. The 60-min integrated plasma gastrin response to beer, red and white wine was about 50% of the gastrin response to the protein-rich (steak) meal (883 +/- 297 pmol X min X 1(-1); mean +/- SE). A drink of 250 ml of white wine together with the meal did not cause a significantly higher integrated gastrin response than the protein meal with 250 ml of distilled water. We conclude that commonly ingested alcoholic beverages such as beer, red and white wine, but not whisky, are potent stimulants of gastrin release in humans. The ethanol content of these beverages cannot be responsible for the increase in plasma gastrin levels, since oral ingestion of pure ethanol in equivalent concentrations and amounts did not elicit a rise in plasma gastrin levels. Some unknown ingredients present in beer and wine are most likely responsible for the gastrin release by both alcoholic beverages.
Adult↗
Excretion of azlocillin and mezlocillin by the normal pancreas and in acute pancreatitis in dogs and rats.
Dogs and rats were studied to evaluate the excretion of two new acyl-ureidopenicillins, azlocillin and mezlocillin, in the pancreatic fluid. After intravenous administration of 55 mg X kg-1 of either drug, an extremely low concentration (less than 3.0 micrograms X ml-1) of both antibiotics was measured in pancreatic juice of conscious dogs. In rats, both azlocillin and mezlocillin were excreted by the pancreas in bactericidal concentrations (greater than 10 micrograms X ml-1) during the first 15 min following their injection. In anesthetized dogs and rats in which acute pancreatitis was induced by injection of sodium taurocholate into the main pancreatic duct, the tissue concentration of mezlocillin (55 mg X kg-1 i.v.) was significantly higher than in the pancreatic tissue of control animals. In both instances, bactericidal concentrations of mezlocillin were measured in the pancreatic tissue. During the first 30 min following its injection, the concentration of mezlocillin was about five times higher in inflammed pancreatic tissue than in the normal pancreas (dogs: 44 +/- 14 vs. 5 +/- 3 micrograms X g-1 tissue; rats: 67 +/- 10 vs. 13 +/- 2 micrograms X g-1). These data indicate that (1) azlocillin and mezlocillin are excreted in bactericidal concentrations by the normal pancreas only in rats but not in dogs, and (2) in both species, bactericidal concentrations of mezlocillin can be observed in the normal pancreatic tissue and in acute pancreatitis; its concentration being significantly higher in acute pancreatitis than in controls.
Acute Disease↗
Effect of atropine on pancreatic bicarbonate output and plasma concentrations of immunoreactive secretin in response to intraduodenal stimulants.
In conscious dogs with gastric and pancreatic Thomas fistulas we studied the effect of atropine (50 micrograms kg-1 intravenously) on pancreatic bicarbonate output and plasma concentrations of immunoreactive secretin in response to intraduodenal bolus injections of HCl (0.75 mmol), L-tryptophan (1 mmol), and sodium oleate (1 mmol). The 10-min integrated bicarbonate response to HCl was 1.7 times greater than the response to oleate and 2.8 times greater than that to tryptophan. Atropine significantly (p less than 0.05) depressed the 10-min integrated bicarbonate response to HCl, oleate, and tryptophan by 67%, 79%, and 61%, respectively. HCl and oleate, but not tryptophan, significantly increased plasma secretin concentrations over basal levels. Atropine did not significantly alter basal plasma concentrations of secretin or the 10-min integrated plasma secretin response to HCl and oleate. We conclude that 1) intraduodenal tryptophan stimulates pancreatic bicarbonate secretion by an atropine-sensitive mechanism, release of secretin not being involved, and 2) in the presence of atropine the depressed pancreatic bicarbonate response to HCl and oleate is not due to decreased release of endogenous secretin.
Animals↗
[What control solutions should be used in studies on the acute effect of alcohol on the gastrointestinal tract?].
There exists still a considerable confusion in the literature about the appropriate control solution for ethanol. In many studies either no control or equimolar solutions of urea, mannitol or sodium chloride were used as an osmotic control for ethanol; distilled water being given only in a few cases. The confusion is mainly derived from the opinion that the osmolality of the ethanol solution as measured by freezing point depression (= "theoretical osmotic pressure") is the determinant factor for the action of ethanol on the gastrointestinal tract. This opinion, however, is not correct. Since biological membranes are not perfectly semipermeable (i. e., they are permeable to certain solutes) the "effective osmotic pressure" produced by permeant solutes is always less than the ("theoretical") osmotic pressure as determined by freezing point depression. The ratio of the "effective" to the "theoretical" osmotic pressure of a solute is defined by the Stavermann reflection coefficient for a certain membrane. The Stavermann reflection coefficient may have any value between 1 and 0. For an impermeant solute the reflection coefficient equals 1 and for increasingly permeant solutes it becomes progressively less than 1 and closer to 0. The Stavermann reflection coefficient of ethanol for some gastrointestinal organs tested is about 0.1. The ideal osmotic control for ethanol would be a solute which exerts the same effective osmotic pressure on the gastrointestinal membrane as ethanol, i. e. which has the same Stavermann reflection coefficient as ethanol, and has no specific pharmacologic effect. Distilled water seems to be the most suitable osmotic control for ethanol because it has a Stavermann reflection coefficient of 0 and has no pharmacological actions.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Does basal cholinergic activity potentiate exogenous secretin for stimulation of pancreatic bicarbonate output in dogs?
In conscious dogs with gastric and pancreatic Thomas fistulas, we studied the effect of atropine sulfate (20 micrograms kg-1 h-1 intravenously) on bicarbonate output basally and in response to intravenous infusion of synthetic secretin (62.5, 125, 250, 500, 1,000 and 2,000 ng kg-1 h-1). We analyzed the data in an attempt to determine whether basal cholinergic activity potentiates the pancreatic bicarbonate response to secretin. Assuming that atropine suppresses all basal cholinergic activity, C (= bicarbonate response to basal cholinergic activity alone) was calculated by subtracting basal pancreatic bicarbonate output with atropine from that without atropine, S (= response to secretin alone) was calculated by subtracting basal pancreatic bicarbonate output with atropine from that in response to secretin with atropine. SwC was defined as the response to secretin acting simultaneously with (w) basal cholinergic activity and was calculated by subtracting basal pancreatic bicarbonate output with atropine from the response to secretin without atropine. If SwC was significantly greater than S + C (= sum of effects of stimulus alone and basal cholinergic activity alone) potentiation between basal cholinergic activity and secretin was assumed to exist. C was 30 +/- 9 mumol 15 min-1 for bicarbonate output. SwC of bicarbonate output was significantly (p less than 0.05) greater than S + C in response to the four lowest doses (62.5-500 ng kg-1 h-1) of secretin. We conclude that potentiation exists between basal cholinergic activity and low doses of exogenous secretin. Thus, basal cholinergic activity is an important modulator of pancreatic bicarbonate response to secretin.
Animals↗
Lack of effect of luteinizing hormone-releasing hormone on pancreatic exocrine secretion and release of gastrin and pancreatic polypeptide in dog.
In 7 conscious dogs with gastric and duodenal Thomas fistulas we studied the effect of an intravenous bolus injection of luteinizing hormone-releasing hormone (LHRH, 100 microgram) on pancreatic bicarbonate and protein secretion stimulated by an intravenous infusion of secretin (500 ng kg-1 hr-1) and on plasma concentrations of pancreatic polypeptide (PP) and gastrin. LHRH did not significantly alter pancreatic bicarbonate and protein output in response to secretion and plasma levels of gastrin and PP as measured by radioimmunoassay. The lack of any significant influences of intravenous LHRH on exocrine pancreatic secretion does not exclude an effect of LHRH on pancreatic bicarbonate and enzyme secretion via paracrine delivery.
Animals↗
[Evidence for the hormonal and nerve regulation of pancreatic secretion: demonstration of an enteropancreatic reflex].
The hypothesis that the pancreatic enzyme response to intestinal stimulants is mediated in part by a vagovagal enteropancreatic reflex was investigated by comparing the effect of intestinal stimulants on the innervated, intact pancreas and the denervated, autotransplanted uncinate process of the pancreas in the same dogs. Furthermore the latency for increase in pancreatic amylase secretion after intraportal injection of cholecystokinin was compared with the latency for the increase in pancreatic amylase secretion after intraduodenal injection of known stimulants of cholecystokinin release. Experiments were done with and without atropine and before and after truncal vagotomy. The results of this study provide strong evidence for the existence of an enteropancreatic reflex.
Amylases↗
Effects of truncal vagotomy and antrectomy on bombesin-stimulated pancreatic secretion, release of gastrin, and pancreatic polypeptide in the anesthetized dog.
The short-term effects of truncal vagotomy and antrectomy on bombesin-stimulated pancreatic secretion and release of gastrin and pancreatic polypeptide (PP) were studied in 18 anesthetized dogs. Together with an intravenous infusion of secretin (250 ng/kg/hr) bombesin (500 ng/kg/hr) was given before and after truncal vagotomy, antrectomy, and sham operation (N = 6 dogs per group). Peak incremental pancreatic protein output in response to bombesin was about 2-3 times higher before than after the different surgical procedures (tachyphylaxis). Neither truncal vagotomy nor antrectomy significantly altered the pancreatic protein response to bombesin when compared with sham operation. Bombesin produced a mean 1-hr increase over basal of 196 pM for gastrin, which was abolished by antrectomy but not appreciably affected by truncal vagotomy and sham operation. The mean 1-hr increment (207 pM) for PP in response to bombesin was not changed by truncal vagotomy, antrectomy, and sham operation. This study shows in the anesthetized dog that exogenous bombesin stimulates release of PP as well as gastrin; that the release of gastrin by bombesin is not vagally dependent; that neither truncal vagotomy nor antrectomy alter the release of PP by bombesin; and that the action of bombesin on pancreatic protein secretion does not depend on release of gastrin or on intact vagal nerves.
Animals↗
Effect of atropine on pancreatic response to HCl and secretin.
In dogs with gastric and pancreatic fistulas, we studied the effect of atropine on the pancreatic secretory response to secretin and intestinal HCl. Atropine sulfate (20 micrograms.kg-1.h-1 iv) significantly depressed basal bicarbonate and protein output. Atropine depressed bicarbonate responses to low doses (62.5, 125, 250, and 500 ng.kg-1.h-1) of secretin but had no significant effect on responses to high doses (1,000 and 2,000 ng.kg-1.h-1). Secretin, with or without atropine, did not stimulate pancreatic protein output above basal. Atropine depressed bicarbonate responses to low loads (3, 6, and 12 mmol.h-1) of HCl but had no significant effect on responses to high loads (12, 24, and 48 mmol.h-1). Intraduodenal HCl produced a dose-dependent increase in protein output. Atropine abolished protein responses to low loads (3 and 6 mmol.h-1) but did not affect responses to high loads (24 and 48 mmol.h-1) of HCl. These findings are compatible with the hypotheses that a) endogenous cholinergic activity augments the pancreatic bicarbonate response to secretin, and b) the pancreatic protein response to intraduodenal HCl is, at least in part, mediated cholinergically.
Animals↗
Effect of adding albumin to solutions of secretin on pancreatic volume and bicarbonate response.
In six conscious dogs with gastric and pancreatic Thomas fistulas, we studied the pancreatic bicarbonate response to intravenous bolus injections of synthetic secretin dissolved either in 5 ml of 0.15 M NaCl alone or in the same amount of NaCl to which dog albumin had been added, to give a 0.1% solution. The pancreatic bicarbonate (micromol . 10 min-1) response to the four lowest doses of secretin (12.5, 25, 50, 100 ng . kg-1) used was significantly (p less than 0.05) higher when secretin was dissolved in NaCl plus albumin than in NaCl alone. The pancreatic response to higher doses of secretin (200, 400, 800, 1600 ng . kg-1) was not significantly altered by the addition of albumin. The D50 of secretin was about 2.6 times greater in the absence than in the presence of albumin. This study suggests that albumin should be added to dilute solutions of secretin to preserve biological activity.
Albumins↗
[Pancreatic polypeptide--a new candidate hormone, physiological and pathophysiological aspects (author's transl)].
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Adenoma, Islet Cell↗
Effect of atropine on secretion from intact and transplanted pancreas in dog.
In dogs with a fistula of the intact pancreas and a transplanted portion of pancreas, we studied the effect of atropine on the pancreatic secretory response to intravenous caerulein and to intestinal perfusion with tryptophan, both given with a secretin background. Atropine (50 micrograms . kg-1 given as an intravenous bolus injection followed by 20 micrograms . kg-1 . h-1 iv infusion) depressed bicarbonate and protein secretion from intact pancreas during stimulation by secretin alone (250 ng . kg-1 . h-1) but did not suppress the increment in bicarbonate secretion in response to caerulein or tryptophan given against the secretin background. In intact pancreas, atropine suppressed protein secretion in response to tryptophan but not in response to caerulein. Atropine had no significant effect on the secretion of bicarbonate and protein from transplanted pancreas in response to secretin, caerulein, or tryptophan. Thus, the only significant effect of atropine on bicarbonate and protein secretion from intact and transplanted pancreas in response to intravenous caerulein or intraduodenal tryptophan, both given against a background of secretin, was inhibition of the protein response to tryptophan in the intact pancreas. These findings are compatible with the hypothesis that pancreatic protein secretion in response to intraduodenal tryptophan is mediated in part by a cholinergic enteropancreatic reflex.
Animals↗