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Biomedical subjects

J B Jansen

Publications and source records attributed to J B Jansen.

At least 271 records · Page 15Linked to original sources
PubMed1986

Physiological role and localization of cholecystokinin release in dogs.

In dogs with pancreatic fistulas, meat feeding and intestinal perfusion with a sodium oleate or amino acid mixture increased pancreatic protein secretion to approximately 110, 100, and 50%, respectively, of the response to cholecystokinin (CCK) at a dose of 85 pmol X kg-1 X h-1. Plasma CCK response increased in these studies to approximately 100, 180, and 40%, respectively, of the value obtained with exogenous CCK, suggesting that, in addition to CCK, other neurohormonal factors contribute to pancreatic enzyme secretion in response to endogenous stimulants. Feeding and duodenal oleate or amino acids also stimulate the release of pancreatic polypeptide (PP), which may be involved in the control of pancreatic secretion in response to endogenous stimulants, including CCK. Perfusion of the intact intestine with graded amounts of oleate (0.5-16 mmol/h) produced dose-dependent increments in plasma CCK and pancreatic protein similar to those obtained with intravenous infusion of graded doses of CCK (0.85-255 pmol X kg-1 X h-1). Oleate perfusion of isolated Thiry loops (30 cm long) made of duodenojejunal (D-J) and ileal (I) segments also stimulated protein secretion but elevated plasma CCK only after perfusion of the D-J but not of the I loop. We conclude that 1) the endogenous CCK released by various luminal stimulants drives the pancreatic protein secretion; 2) the release of CCK is confined to the foregut; and 3) PP concomitantly released by various intestinal stimulants may contribute to the control of pancreatic secretion induced by endogenous CCK.

Animals↗
PubMed1985

Physiological plasma concentrations of cholecystokinin stimulate pancreatic enzyme secretion and gallbladder contraction in man.

The present study was undertaken to determine whether infusion of cholecystokinin (CCK) to plasma concentrations comparable to those found after a meal stimulates pancreatic enzyme secretion and gallbladder contraction. Plasma CCK concentrations were measured by radioimmunoassay using antibody T204, which binds to all carboxyl-terminal CCK-peptides containing the sulfated tyrosine region. Ingestion of a standardized test meal in 7 normal subjects induced significant increases in plasma CCK from 2.0 +/- 0.2 pmol/l to levels between 4.6 +/- 0.6 and 7.3 +/- 1.0 pmol/l (p less than 0.05-p less than 0.0005). Infusion of 2.5 pmol/kg X h CCK 33 resulted in significant increases in plasma CCK from 2.0 +/- 0.2 to 3.9 +/- 0.3 pmol/l (p less than 0.0005). This infusion of CCK induced significant increases in trypsin secretion from 0.5 +/- 0.1 to 1.4 +/- 0.2 KU/15 min (p less than 0.005) and in bilirubin output from 1.6 +/- 0.7 to 30.3 +/- 8.0 mumol/15 min (p less than 0.05). It is concluded that physiological plasma concentrations of CCK stimulate pancreatic enzyme secretion and gallbladder contraction in man.

Adult↗
PubMed1985

Effect of graded physiologic doses of cholecystokinin on gallbladder contraction measured by ultrasonography. Determination of threshold, dose-response relationships and comparison with intraduodenal bilirubin output.

This study was undertaken to determine in healthy humans the effect of graded physiologic doses of cholecystokinin (CCK) on gallbladder size as assessed by ultrasonography and to analyze the relations between the doses of CCK infused, the plasma CCK increments, the decreases in gallbladder volume, and the cumulative intraduodenal bilirubin output. Infusion of stepwise-increasing doses of CCK, ranging from 0.2 to 6.4 pmol/kg X h, induced dose-related increases in plasma CCK (r = 0.99; p less than 0.001), decreases in gallbladder volume (r = 0.99; p less than 0.001), and increases in intraduodenal bilirubin output (r = 0.96; p less than 0.01). There was a highly significant correlation between the decreases in gallbladder volume and the cumulative intraduodenal bilirubin outputs (r = 0.98; p less than 0.001). Infusion of 0.8 pmol/kg X h of CCK, resulting in an increase in plasma CCK of 1.3 +/- 0.5 pmol/L, was the threshold for stimulating gallbladder contraction as assessed by both ultrasonography and measurement of intraduodenal bilirubin output. It is concluded that ultrasonography is a sensitive method for the quantitation of gallbladder contraction and that physiologic plasma CCK concentrations do stimulate gallbladder contraction.

Adult↗
PubMed1985

Effect of medium-chain triglycerides and long-chain triglycerides on plasma pancreatic polypeptide secretion in man.

Since it has been shown that stimulation of pancreatic enzyme secretion by triglycerides is dependent on the chain length of the fatty acids, we have studied whether the secretion of pancreatic polypeptide (PP) in response to triglycerides is also related to the chain length of the fatty acids. Therefore, the effect of equimolar amounts (60 mmol) of medium-chain triglycerides (MCT) and long-chain triglycerides (LCT) on plasma PP was studied in 6 normal subjects. In the control study the subjects ingested 60 ml of 0.15 mol/l saline. Ingestion of LCT resulted in significant increases in plasma PP from 33 +/- 7 to 55 +/- 7 pmol/l (P less than 0.01), whereas both MCT and saline did not significantly increase plasma PP concentrations. Similarly, the integrated plasma PP secretion after LCT (1022 +/- 392 pmol/l per 90 min) was significantly greater than that after MCT (-690 +/- 358 pmol/l per 90 min; P less than 0.001) and that after saline (-462 +/- 205 pmol/l per 90 min; P less than 0.01). It is concluded that the secretion of PP in response to triglycerides is dependent on the chain length of the fatty acids.

Administration, Oral↗
PubMed1985

Effects of acute hypercalcemia on exocrine pancreatic secretion in the cat.

To investigate the effects of acute hypercalcemia on exocrine pancreatic secretion, anesthetized cats were given calcium intravenously. Increasing hypercalcemia (3.7-6.3 mmol/L) evoked a dose-dependent increase in enzyme output that was 12 times greater than in normocalcemic controls (p less than 0.001) and was 60% of subsequent maximal stimulation with intravenous cholecystokinin (CCK). The effect of hypercalcemia on enzyme secretion was abolished when CCK was administered 60 min before calcium and at a dose to cause maximal enzyme output. Atropine did not prevent the calcium-induced increase in enzyme secretion. Pancreatic fluid and bicarbonate outputs were not influenced by hypercalcemia during intravenous administration of small amounts of secretin, but were increased by addition of CCK to the secretin infusion. Hypercalcemia did not induce macroscopic or light-microscopic changes in pancreatic morphology. Plasma levels of both CCK and gastrin were increased (p less than 0.01) during hypercalcemia, with and without precalcium administration of CCK; atropine significantly inhibited (p less than 0.05), but did not abolish the calcium-induced releases of both peptides. These data suggest that in the anesthetized cat, acute hypercalcemia induced by intravenous calcium infusion stimulates pancreatic secretion of enzymes, but not fluid and bicarbonate. Acute hypercalcemia also causes release of CCK and, as shown previously, gastrin. The findings suggest that the stimulatory effect of hypercalcemia on pancreatic enzyme secretion is not dependent on intact cholinergic pathways and is probably not exclusively mediated by release of CCK or gastrin.

Acute Disease↗
PubMed1985

Gallbladder contraction: effects of fatty meals and cholecystokinin.

Gallbladder contraction and hormone release were measured in six healthy volunteers after their ingestion of two commercially available fatty meals (Biloptin Fatty Meal and Sorbitract) and intravenous bolus injection of 1 Ivy Dog Unit/kg body weight cholecystokinin (CCK) to compare the effectiveness of fatty meals to CCK. Differences in gallbladder volumes, rate constants of emptying, and times of maximal contractions, as measured by real-time sonography, were not statistically significant. Peak levels of CCK, a potent stimulant of gallbladder contraction, and of pancreatic polypeptide, an inhibitor of gallbladder contraction, were significantly higher (P less than .05-P less than .005) after administration of CCK than after ingestion of each fatty meal, but this did not significantly affect emptying rate or maximal contraction. We conclude that the use of intravenous CCK does not offer any advantage over the ingestion of fatty meals in radiographic studies of gallbladder involving induced contractions.

Adult↗
PubMed1985

Pancreatic enzyme response to a liquid meal and to hormonal stimulation. Correlation with plasma secretin and cholecystokinin levels.

Pancreatic trypsin output and plasma secretin and cholecystokinin (CCK) levels were measured in five healthy volunteers to investigate the mechanisms involved in regulating postprandial pancreatic secretion. The pancreas was stimulated by a liquid test meal or by either intravenous secretin (1-82 pmol/kg-1 per h-1) or caerulein, a CCK analogue (2.3-37 pmol/kg-1 per h-1), or by a combination of secretin and caerulein. Pancreatic secretion was assessed by a marker perfusion technique (polyethylene glycol [PEG 4000]), plasma secretin, and CCK by specific radioimmunoassays. Increasing doses of secretin produced increasing bicarbonate output (P less than 0.01), whereas trypsin was not stimulated over basal. Graded caerulein produced a stepwise increase in trypsin and bicarbonate output (P less than 0.01). Potentiation occurred for bicarbonate secretion between secretin and caerulein, but not for trypsin output. Postprandial trypsin secretion averaged 29.1 IU/min-1 over 150 min (equal to 55% of maximal response to caerulein). The peak trypsin response amounted to 90% of maximal caerulein. Significant increases of plasma secretion (P less than 0.05) and CCK (P less than 0.01) were observed after the meal. Comparison of enzyme and CCK responses to the testmeal or to exogenous caerulein suggested that the amount of CCK released after the meal could account for the postprandial trypsin secretion. We conclude that (a) the postprandial enzyme response in man is submaximal in comparison to maximal exogenous hormone stimulation; (b) CCK is a major stimulatory mechanism of postprandial trypsin secretion, whereas secretin is not involved; and (c) Potentiation of enzyme secretion is not a regulatory mechanism of the postprandial secretory response.

Adult↗
PubMed1985

Comparative study of the effects of equal amounts of fat, protein, and starch on plasma cholecystokinin in man.

The effect of ingestion of 50 g fat, 50 g protein, and 50 g starch on plasma cholecystokinin (CCK) concentrations was studied in eight healthy volunteers. Plasma CCK concentrations were measured by radioimmunoassay with Bolton-Hunter-labelled CCK 33, CCK 33 standard, and antibody T204. Antibody T204 was directed to the sulphated tyrosine region of CCK. Ingestion of fat and protein induced significant increases in plasma CCK, whereas ingestion of starch did not significantly influence plasma CCK levels. Peak increments in plasma CCK after fat (4.8 +/- 0.9 pmol/l) and protein (3.4 +/- 0.5 pmol/l) were significantly greater than that after starch (0.9 +/- 0.3 pmol/l). Similarly, the integrated plasma CCK secretion after fat (213 +/- 49 pmol/l X 120 min) and after protein (178 +/- 53 pmol/l X 120 min) was significantly greater than that found after ingestion of starch (9 +/- 23 pmol/l X 120 min). It is concluded that, in contrast to starch, fat and protein are potent stimuli for the release of CCK.

Adult↗
PubMed1984

Characterization of antisera to cholecystokinin by use of different cholecystokinin labels.

Antisera raised against synthetic sulphated cholecystokinin (CCK 26-33) (n = 4) and against 30% pure porcine CCK (n = 11) were characterized by the use of different labelled CCK peptides. CCK 39 and CCK 26-33 were coupled to 125I by the chloramine-T method, while CCK 33 was conjugated to 125I-labelled hydroxyphenylpropionic acid-succinimide ester (Bolton-Hunter reagent). Antisera raised against CCK 26-33 bound to 125I-CCK 26-33 only. Of the antisera raised against 30% pure CCK, 2 bound to all 3 labels, 4 to 125I-BH-CCK 33 and 125I-CCK 26-33, 3 to 125I-CCK 39 and 125I-BH-CCK 33, 1 to 125I-CCK 26-33 only and 1 to 125I-BH-CCK 33 only. The antibodies reacting with 125I-CCK 26-33 bound also to 125I-gastrin 1-17. Different CCK labels bound to different binding sites in the same antiserum (antibody heterogeneity). The pattern of reactivity of the antiserum to CCK peptides was dependent on the type of label used. With these different labels, antibodies specific for CCK 39, for CCK 33 and CCK 39, for sulphated forms of CCK, and for all CCK peptides and gastrin could be detected. It is concluded that antisera raised against CCK should be characterized by use of different labelled CCK materials.

Animals↗
PubMed1984

Omeprazole in Zollinger-Ellison syndrome. Effects of a single dose and of long-term treatment in patients resistant to histamine H2-receptor antagonists.

We studied the effect of omeprazole, a benzimidazole inhibitor of gastric acid secretion, in patients with Zollinger-Ellison syndrome. In five patients ingestion of 80 mg of omeprazole inhibited gastric acid secretion by 26 to 100 per cent after 6 hours and by 76 to 100 per cent after 24 hours. Seven patients were continuously treated with omeprazole once or twice daily for 8 to 19 months (average, 14). Six of these seven had symptoms that were resistant to high doses of histamine H2-receptor antagonists, and the seventh could not take high doses of cimetidine because of a possible drug-related increase in the serum creatinine concentration. Symptoms resolved in all patients within two weeks, and peptic lesions were healed at endoscopy after four weeks. All patients remained free of symptoms, and gastric acid secretion continued to be markedly inhibited by omeprazole therapy. We conclude that omeprazole is a potent and long-acting antisecretory drug in patients with Zollinger-Ellison syndrome and that it is effective in patients whose peptic-ulcer disease is relatively resistant to treatment with histamine H2-receptor antagonists. Its safety and effectiveness in long-term therapy remain to be assessed.

Adult↗
PubMed1984

Serum trypsin, alpha-amylase and lipase during bombesin stimulation in normal subjects and patients with pancreatic insufficiency.

The effect of infusion of bombesin (60 pmol/kg 20 min) on pancreatic enzymes in serum was studied in 13 normal subjects and 12 patients with pancreatic insufficiency. In normal subjects administration of bombesin induced large increases in serum trypsin (p less than 0.01), while serum total alpha-amylase and pancreatic alpha-amylase did not change and serum lipase showed only a modest rise (0.01 less than p less than 0.05). Patients with pancreatic insufficiency had significantly lower serum concentrations of all enzymes studied (p less than 0.01) and in such patients bombesin did not change the concentrations of pancreatic enzymes in serum. It is concluded that determination of the serum trypsin response to bombesin may be of help in the diagnosis of pancreatic insufficiency.

Adolescent↗
PubMed1984

Comparative study of plasma pancreatic polypeptide responses to food, secretin, and bombesin in normal subjects and in patients with chronic pancreatitis.

Plasma pancreatic polypeptide (PP) responses to food, secretin (1 CU/kg, intravenous) and bombesin (60 pmol/kg/20 min intravenous) were compared in 14 normal subjects and in 17 patients with chronic pancreatitis and pancreatic insufficiency. Basal plasma PP concentrations were significantly higher in normal subjects than in patients with chronic pancreatitis, but there was considerable overlap between the groups. Ingestion of food induced significant increases in plasma PP both in normal subjects and in patients with chronic pancreatitis, whereas secretin and bombesin significantly increased plasma PP levels in normal subjects only. The PP responses to the three stimuli were significantly larger in normal subjects than in patients with chronic pancreatitis, but there was marked overlap. Calculation of the peak to basal plasma PP ratio did not result in better discrimination between the two groups. In normal subjects there were no significant correlations between the PP responses to the three stimuli, whereas in patients with chronic pancreatitis these responses were significantly correlated. Furthermore, in patients with chronic pancreatitis the PP responses to the various stimuli were significantly correlated with the basal plasma PP level.

Adolescent↗