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Biomedical subjects

J B Jansen

Publications and source records attributed to J B Jansen.

At least 109 records · Page 6Linked to original sources
PubMed1994

Loxiglumide inhibits cholecystokinin stimulated somatostatin secretion and simultaneously enhances gastric acid secretion in humans.

In vitro studies have demonstrated that cholecystokinin releases somatostatin from the gastric mucosa. To date, there is no information about the in vivo significance of this finding in man. Therefore, we have studied the effect of infusion of cholecystokinin resulting in plasma concentrations within the range found after meal-stimulation, on somatostatin release and on gastric acid secretion. In addition we have studied these functions during infusion of the type A cholecystokinin receptor antagonist loxiglumide. In eight healthy subjects, basal gastric acid secretion was distinctly stimulated by cholecystokinin. The effect of cholecystokinin on gastric acid secretion was markedly enhanced by loxiglumide. Cholecystokinin also significantly stimulated somatostatin output into the gastric lumen, but not into the systemic circulation. Somatostatin output into the gastric lumen during infusion of cholecystokinin was abolished by loxiglumide. The data indicate that on the one hand circulating cholecystokinin, like gastrin, stimulates gastric acid secretion probably by binding to less specific type B receptors on parietal cells that are not blocked by loxiglumide, but on the other hand that cholecystokinin, in contrast to gastrin, also inhibits gastric acid secretion probably by binding to specific type A receptors present on somatostatin producing D-cells in the gastric mucosa, that are blocked by loxiglumide.

Adult↗
PubMed1994

Long-term treatment with omeprazole for refractory reflux esophagitis: efficacy and safety.

OBJECTIVE: To evaluate the long-term efficacy and safety of omeprazole in patients with gastroesophageal reflux disease resistant to treatment with histamine-2 (H2)-receptor antagonists. DESIGN: Cohort analytic study with a mean follow-up of 48 months (range, 36 to 64 months). SETTING: Patients receiving ambulatory care from referral centers. PATIENTS: 91 patients with gastroesophageal reflux disease resistant to treatment with an H2-receptor antagonist but subsequently responsive to 40 mg of omeprazole daily. INTERVENTION: Open maintenance therapy consisting of 20 mg of omeprazole daily in 86 patients and 40 mg daily in 5 patients. OUTCOME MEASURES: Endoscopy to assess healing; side effects, laboratory values, fasting serum gastrin level, and gastric corpus biopsies to assess safety. RESULTS: Esophagitis recurred in 47% of the patients receiving 20 mg of omeprazole daily, but all rehealed after the dose was doubled. Seven of 40 patients (18%) had a second relapse after a mean follow-up time of 24 months (range, 9 to 36 months) that was successfully treated with a further 20-mg dose increment for a mean period of 36 months (range, 6 to 39 months). Median gastrin levels increased initially from 60 ng/L before study entry to 162 ng/L (P < 0.01) with treatment and reached a plateau during maintenance treatment. Very high gastrin levels (> 500 ng/L) were observed in a subgroup (11%) of patients. The incidence of micronodular hyperplasia increased from 2.5% of the patients at first biopsy to 20% at the last biopsy (P = 0.001), with a corresponding progression of gastritis to subatrophic or atrophic gastritis from less than 1% to 25% (P < 0.001), which was more pronounced in patients with very high serum gastrin levels. CONCLUSIONS: Maintenance therapy with omeprazole was effective for at least 5 years in patients with gastroesophageal reflux disease resistant to treatment with H2-receptor antagonists. Treatment was accompanied by a persistent increase in serum gastrin levels and an increase of micronodular argyrophil cell hyperplasia and subatrophic or atrophic gastritis.

Barrett Esophagus↗
PubMed1994

Foetor hepaticus.

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Breath Tests↗
PubMed1994

Effect of hyperglycaemia on gallbladder motility in type 1 (insulin-dependent) diabetes mellitus.

Patients with diabetes mellitus are at increased risk of developing gallstones. This has been attributed, among other factors, to alterations in gallbladder motility in the presence of autonomic neuropathy. Since high blood glucose concentrations impair gastric emptying in diabetic patients, we have investigated the effect of acute hyperglycaemia on gallbladder motility. Seven Type 1 (insulin-dependent) diabetic patients were studied twice during euglycaemia (blood glucose 5 mmol/l) and hyperglycaemia (blood glucose 15 mmol/l) using a clamp technique. In addition, seven healthy volunteers were studied during euglycaemia and hyperglycaemia. Gallbladder volumes, measured with ultrasonography, were studied before and during infusion of step-wise increasing doses of cholecystokinin-33, 0.25, 0.5 and 1.0 Ivy Dog Unit.kg-1.h-1, each dose for 30 min. Mean basal gallbladder volumes were not significantly different in the four experiments. Administration of cholecystokinin resulted in significant (p < 0.05) dose-dependent reductions in gallbladder volume in all experiments. During euglycaemia the gallbladder contraction in diabetic patients was not significantly different from the control subjects. During hyperglycaemia the gallbladder contraction in the diabetic patients was significantly (p < 0.05) reduced compared to euglycaemia only during infusion of 0.25 Ivy Dog Unit.kg-1.h-1 of cholecystokinin (19 +/- 6% vs 33 +/- 6%). Compared to euglycaemia, during hyperglycaemia the gallbladder contraction in the control subjects was significantly (p < 0.05) reduced during infusion of 0.25, 0.5 and 1.0 Ivy Dog Unit.kg-1.h-1 of cholecystokinin (14 +/- 4% vs 31 +/- 3%; 42 +/- 6% vs 65 +/- 5%; 74 +/- 4% vs 90 +/- 3%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Relation between gastric emptying of albumin-dextrose meals and cholecystokinin release in man.

The effect of intragastric dextrose on albumin-stimulated cholecystokinin (CCK) release was studied in five healthy subjects and was related to gastric emptying and pancreatobiliary secretions. When combined with low concentrations of dextrose (4 g/100 ml), a 500-ml solution of albumin (7 g/100 ml) was rapidly emptied from the stomach into the duodenum (T1/2: 35 min). This rapid gastric emptying resulted in an only transient stimulation of pancreatobiliary secretion and an integrated CCK release of 278 +/- 45 pM x 180 min. When the concentration of dextrose in the albumin solution was increased from 4 g/100 ml to 21 g/100 ml, gastric emptying rate was distinctly slower (T1/2: 78 min; P < 0.01) and pancreatobiliary secretions became sustained (P < 0.01). CCK release was markedly higher (900 +/- 421 pM x 180 min; P < 0.05) after ingestion of the solution containing a high dextrose concentration. Intraduodenal infusion of 21 g/100 ml dextrose (3.1 ml/min) failed to significantly stimulate plasma CCK levels (119 +/- 38 pM x 120 min). We suggest that the higher CCK release in response to intragastrically administered albumin solution containing high concentrations of dextrose may have been induced by augmented peptic digestion of albumin due to delayed gastric emptying and by increased enteral digestion of albumin due to increased pancreatobiliary outputs.

Adult↗
PubMed1994

Effect of synthetic prostaglandin E2 analog enprostil on omeprazole-induced hypergastrinemia and hyperpepsinogenemia.

This study was undertaken to determine whether the synthetic prostaglandin E2 analog enprostil is able to inhibit basal and postprandial hypergastrinemia induced by omeprazole. We also studied the effect of omeprazole, enprostil, and the combination of both drugs on serum pepsinogen A and C levels. Eight normal subjects received in random order five-day courses of 40 mg omeprazole once a day, 35 micrograms enprostil three times a day, the combination of both drugs, and placebo. Omeprazole induced significant increases in basal and postprandial serum gastrin and in pepsinogen A and C levels. These increments persisted on the day after stopping treatment. Coadministration of enprostil inhibited omeprazole-induced basal hypergastrinemia and postprandial integrated serum gastrin, but not basal serum pepsinogen A and C, while the inhibition on the day after the treatment courses only reached statistical significance for the postprandial integrated serum gastrin concentration. It is concluded that enprostil inhibits omeprazole-induced basal and postprandial hypergastrinemia, with a tendency to protracted inhibition after stopping the drugs, and that enprostil does not significantly influence omeprazole-induced increases in pepsinogen A and C level. Coadministration of enprostil may be helpful in preventing pronounced hypergastrinemia in the few patients who show large serum gastrin increases during treatment with omeprazole.

Adult↗
PubMed1994

Effect of intravenous glucose on intravenous amino acid-induced gallbladder contraction and CCK secretion.

The present study was undertaken to investigate the effect of acute hyperglycemia on the gallbladder contraction induced by intravenous administration of high doses of amino acids (Vamin 18, 250 mg protein/kg/hr). Six healthy volunteers were studied in random order on two occasions during normoglycemia and hyperglycemia with blood glucose levels stabilized at 15 mmol/liter. Gallbladder volumes, measured with ultrasonography, were studied for 60 min before and for 120 min during intravenous infusion of amino acids (IVAA). Administration of IVAA resulted in a significant reduction (P < 0.05) in gallbladder volume from 32 +/- 5 cm3 to 17 +/- 2 cm3 during normoglycemia. During hyperglycemia no significant changes in gallbladder volume were observed in response to IVAA. No significant changes in plasma CCK concentration, the major hormonal stimulus for gallbladder contraction, occurred in response to IVAA. During hyperglycemia, pancreatic polypeptide (PP) secretion, as an indirect measure of vagal cholinergic tone, in response to IVAA was significantly (P < 0.05) reduced compared to normoglycemia. It is concluded that: (1) administration of high doses of IVAA results in significant gallbladder contraction, (2) high doses of IVAA do not stimulate CCK secretion, (3) acute hyperglycemia inhibits IVAA-induced gallbladder contraction, and (4) acute hyperglycemia inhibits basal and stimulated plasma PP secretion, suggesting impaired vagal-cholinergic tone during hyperglycemia.

Adult↗
PubMed1994

A prospective study of effects of Belsey MK IV antireflux surgery on endoscopic esophagitis, lower esophageal sphincter pressure, and 24-hr pH measurements. Relation to symptom improvement.

A prospective study on the effect of the Belsey MK IV operation on esophagitis, lower esophageal sphincter pressure (LESP), and acid reflux as monitored on 24-hr pH recording was conducted to investigate the association between objective changes and the effect of operation on reflux-associated symptoms. Thirty-one patients were included. The effect of surgery on symptoms was recorded in all patients, and 22 patients agreed to undergo endoscopy, manometry, and 24-hr pH recording. Follow-up ranged from three to nine years (mean five years); 87% reported long-lasting improvement (50% free of symptoms, 37% major improvement, no medication needed). The combination of symptomatic improvement and absence of esophagitis was found in 70%. LESP significantly increased [8 +/- 6 mm Hg preoperatively, 14 +/- 5 mm Hg postoperatively (P < 0.001)] to a level above 5 mm Hg in 96% of the patients. No endoscopic esophagitis was found in 17 of 20 patients (85%; P < 0.05) (two patients refused endoscopy). The 24-hr pH monitoring normalized in 11 of the 20 patients (55%) (one registration failed). The operation-induced rise in LESP correlated with improvement on endoscopy (r = 0.51; P < 0.002) and with reduction of reflux parameters (number of episodes with pH < 4: r = 0.64; P < 0.05, percentage of total time pH < 4: r = 0.42; P = 0.07). A rise in LESP must be an important aim of antireflux surgery. The Belsey MK IV does not induce a rise to a level that causes severe dysphagia or bloating, but the trade-off is less control of acid reflux.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Satiety effects of cholecystokinin in humans.

BACKGROUND/AIMS: Cholecystokinin (CCK) inhibits gastric emptying and may exert satiety effects in several species, including humans. Because the effects of physiological doses of CCK on satiety in humans is unclear, the satiety effects of CCK-33 in physiological levels in lean and obese subjects were studied. METHODS: CCK-33 was infused intravenously to 32 healthy men or women (14 obese, all women; 18 lean, 4 men and 14 women) in doses that elicited plasma CCK concentrations in the physiological range. The effects of these infusions on feelings of hunger, wish to eat, fullness, and prospective feeding intentions were measured on visual analogue scales and compared with saline during a 1-hour infusion period. RESULTS: The CCK infusions induced significant decreases in hunger feelings, wish to eat, and prospective feeding intentions (P < 0.05), whereas fullness tended to be increased (P = 0.054). No clear differences between lean and obese subjects were observed apart from a more marked decrease in fullness and increase in prospective feeding intentions during the 1-hour saline infusion in the lean group (P < 0.05). CONCLUSIONS: CCK infusion leading to physiological plasma levels significantly increases satiety in humans.

Adult↗
PubMed1994

Effect of bile salt binding or protease inactivation on plasma cholecystokinin and gallbladder responses to bombesin.

BACKGROUND/AIMS: Bombesin-stimulated plasma cholecystokinin levels decrease after an initial increase despite continuous infusion of bombesin. The aim of this study was to determine if a feedback mechanism, mediated by bile salts or proteolytic enzymes, is responsible for this decline. METHODS: Bombesin (1.0 ng.kg-1.min-1) was infused into volunteers for 180 minutes on separate occasions. Cholestyramine, colestipol, camostate, or saline were perfused intraduodenally during the second hour of the tests. Cholestyramine was also administered without infusion of bombesin. RESULTS: Colestipol and cholestyramine, dependent on their bile salt-binding capacity, markedly enhanced (P < 0.05) bombesin-stimulated plasma cholecystokinin from 2.1 +/- 0.5 pmol/L to 6.4 +/- 2.2 pmol/L and 12.1 +/- 3.3 pmol/L (P < 0.05 vs. colestipol), respectively, and further decreased gallbladder volume (P < 0.05) from 9.4 +/- 1.6 mL to 2.0 +/- 0.4 mL and 2.2 +/- 0.5 mL, respectively. The protease inhibitor camostate had no effect. Bile salt precipitation also enhanced plasma pancreatic polypeptide responses (P < 0.01) but did not alter gastrin responses. Plasma cholecystokinin responses to cholestyramine without bombesin infusion varied considerably, but increments were highly correlated to decreases in gallbladder volume (r = 0.91; P < 0.005). CONCLUSIONS: Bile salt sequestration but not protease inactivation enhances plasma cholecystokinin and gallbladder responses to bombesin infusion in humans.

Adult↗
PubMed1994

The in-vitro uptake of zinc by blood cells in rats with long-term inflammatory stress.

The aim of the present study was to investigate the in vitro uptake of zinc by blood cells, in an attempt to distinguish between those conditions in which low plasma zinc concentrations are due to inflammatory stress, and those which are due to true zinc deficiency. Inflammation induced by intramuscular injection of turpentine caused a significant reduction in plasma albumin concentrations, which persisted until the end of the study (2 weeks). It also caused a reduction in the plasma zinc concentration which was most marked during the first few days. A smaller difference persisted until the end of the study. When the serum zinc concentration was corrected for the hypoalbuminaemia, the changes in serum zinc concentration after the first 4 days of turpentine were small and mainly non-significant. The in vitro uptake of zinc by erythrocytes obtained from animals with inflammation did not increase, whereas the uptake was increased in cells obtained from animals with true zinc deficiency. Therefore this study suggests a method that can probably differentiate between an apparent zinc deficiency due to inflammatory stress and a real zinc deficiency, but additional experiments to validate this method should be performed.

Journal Article↗
PubMed1994

Contemporary radiological examination of the small bowel.

There are clinical data suggesting that the intubation method (enteroclysis) is the most accurate form of examining the small bowel. The diagnostic accuracy of small bowel enema is generally found superior to that of the tubeless method. Despite the growing interest in small bowel enema this procedure has not yet become the prevailing method in Western countries. However, due to further developments in sonde or push enteroscopy in which 300 cm of the small bowel can be visualized, it is of utmost importance to perform state of the art radiological small bowel enteroclysis investigation, otherwise the bright lights from enteroscopy will rapidly illuminate the dark corners of the small intestine, leaving no place for radiology.

Barium Sulfate↗
PubMed1994

Effect of enprostil on serum gastrin and pepsinogen A and C levels in patients on long-term treatment with omeprazole.

BACKGROUND: Treatment of omeprazole induces profound inhibition of gastric acid secretion, resulting in hypergastrinaemia. In rats hypergastrinaemia induced by chronic administration of high doses of omeprazole resulted in ECL-cell hyperplasia and subsequent carcinoid formation. This finding may limit long-term therapy in man. The synthetic prostaglandin E2 analogue enprostil not only inhibits gastric acid secretion but also reduces serum gastrin in normal subjects and in peptic ulcer patients. The present study was undertaken to determine whether enprostil reduces serum gastrin in patients on long-term treatment with omeprazole. METHODS: Eight patients with reflux oesophagitis treated with 40 mg omeprazole once daily for at least 3 months received 35 micrograms enprostil t.d.s. during a 5-day treatment course. Basal and postprandial serum gastrin concentrations and pepsinogen A and C levels were measured on the day before, the first and the final day, and on the day after cessation of treatment. RESULTS: Enprostil significantly (P < 0.05) reduced basal serum gastrin from 65 +/- 15 pmol/L to 51 +/- 13 pmol/L on the first treatment day, and to 41 +/- 9 pmol/L on the final day. Enprostil also significantly (P < 0.05) reduced postprandial integrated serum gastrin from 6173 +/- 849 pmol.h/L to 4516 +/- 906 pmol.h/L and to 3532 +/- 706 pmol.h/L on the first and final treatment days, respectively. On the day after cessation of treatment basal (57 +/- 11 pmol/L) and postprandial integrated serum gastrin concentrations (5766 +/- 864 pmol.h/L) were not significantly different when compared to pretreatment values. Enprostil had no significant influence on serum pepsinogens A and C. CONCLUSION: Short-term co-administration of enprostil lowers the serum gastrin levels in patients on long-term treatment with omeprazole.

Aged↗
PubMed1994

Basal serum gastrin concentrations before and after eradication of Helicobacter pylori infection measured by sequence specific radioimmunoassays.

BACKGROUND: Helicobacter pylori infection of the antral mucosa is responsible for an increase in basal and stimulated serum gastrin. In the present study we have investigated whether gastritis induced by H. pylori is responsible for abnormalities in the processing of gastrin in dyspeptic patients. METHODS: Basal serum gastrin was measured by radioimmunoassay before, 5 weeks, and 1 year after anti-H. pylori therapy in 73 H. pylori positive functional dyspeptic patients. Three region-specific antisera were used, specific for the biologically active carboxy-terminal part, the biologically inactive amino-terminal part of gastrin 1-17, and for the non-sulphated tyrosyl residue in gastrin 1-17. RESULTS: Basal serum gastrin levels were markedly (P < 0.01) decreased 5 weeks and 1 year after successful eradication of H. pylori (n = 39) but not in the patients in whom treatment failed (n = 34). A decline of gastrin was observed for each of the three radioimmunoassays. CONCLUSION: The decrease of serum gastrin levels in all three radioimmunoassays after a successful eradication of H. pylori does not point to major changes in the processing of gastrin. These results suggest that G-cells in the antral mucosa are not functionally affected by the inflammation.

Adult↗
PubMed1994

Effect of a low dose of intraduodenal fat on satiety in humans: studies using the type A cholecystokinin receptor antagonist loxiglumide.

Satiation, the process that brings eating to an end, and satiety, the state of inhibition over further eating, may be influenced by cholecystokinin (CCK). In animal and human studies, it has been shown that infusion of exogenous CCK decreases food intake, but the doses given may well have led to supraphysiological plasma concentrations. This study was done to discover if a low dose of intraduodenal fat releasing physiological amounts of endogenous cholecystokinin exerts satiation or satiety effects, or both and if these effects could be inhibited by the CCK receptor antagonist loxiglumide. In 10 healthy lean volunteers (5 F, 5 M, mean age 26) three tests were performed in a randomised blind fashion. Intralipid 20% (6 g/h) (experiments A and C) or saline (experiment B) were given intraduodenally from 1030 until 1300. The subjects received saline (experiments A and B) or loxiglumide (experiment C) a specific CCK-receptor antagonist (10 mg/kg/h) intravenously from 0930 until 1300. At 1200 a meal was served. At regular time intervals hunger feelings were measured using visual analogue scales and food selection lists and plasma CCK was measured by radioimmunoassay. Food intake (mean (SEM)) during intraduodenal fat (206(35)g) was lower than in the control study (269(37)g, p = 0.09). Loxiglumide largely prevented the inhibitory effect of intraduodenal fat on food intake (245(30)g). From 1030 until the meal at 1200 there was a significant satiating effect of intraduodenal fat compared with the control and loxiglumide experiments according to the food selection lists, which was because of the satiating effect for the fat rich items (p<0.05). Also feelings of fullness were significantly higher during intraduodenal fat than in the control or loxiglumide experiments (p<0.05). During intraduodenal fat there was a significant increase of plasma CCK from 2.4(0.3) to 4.8(0.4) pM (p<0.001). Loxiglumide led to an exaggerated CCK release to a peak concentration of 16(2.4) pM before the meal. This study shows that in humans low dose intraduodenal fat increases satiety and satiation, mainly through the effect of CCK.

Adult↗
PubMed1994

Effect of erythromycin on pancreatic polypeptide release: role of the vagal nerve.

To determine whether long vagal cholinergic pathways are involved in erythromycin-induced pancreatic polypeptide release, erythromycin was administered as an intravenous bolus injection to 9 healthy volunteers (group A) and to 13 patients (group B) with impaired vagal function as a result of truncal vagotomy or accidental vagotomy after antireflux surgery. In 7 of these patients (group B1) an antrectomy was also performed, while in the other 6 patients (group B2) the antrum was not removed. Pancreatic polypeptide was measured by radioimmunoassay at 5-min intervals twice before and at 2, 5, 10, 15, 30, 45 and 60 min after a 3.5 mg/kg bolus injection of erythromycin. On another day, a standard meal was administered and plasma pancreatic polypeptide was measured at 10-min intervals for 1 h. Erythromycin injection resulted in a lower integrated pancreatic polypeptide response in the patients of group B1 (247 +/- 89 pmol/l x 15 min; p = 0.005) and group B2 (497 +/- 111 pmol/l x 15 min; p = 0.05) when compared to the healthy subjects of group A (1,136 +/- 227 pmol/l x 15 min). The pancreatic polypeptide response to erythromycin in group B1 was reduced when compared to group B2, but the difference just failed to reach statistical significance (0.05 < p < 0.10). In the first 30 min after ingestion of a meal (cephalic phase) pancreatic polypeptide release was also markedly lower in group B1 (1,461 +/- 304 pmol/l x 30 min; p < 0.005) and group B2 (1,452 +/- 215 pmol/l x 30 min; p < 0.005) when compared to group A (3,541 +/- 452 pmol/l x 30 min).(ABSTRACT TRUNCATED AT 250 WORDS)

Depression, Chemical↗