PubMed Health⌕ Search

Biomedical subjects

A A Masclee

Publications and source records attributed to A A Masclee.

At least 109 records · Page 6Linked to original sources
PubMed1995

Effect of erythromycin on gallbladder emptying in patients with antrectomy or truncal vagotomy.

OBJECTIVES: Erythromycin, a motilin-like agent, stimulates gallbladder contraction in healthy control subjects. Because the action of erythromycin is cholinergic dependent and possibly related to premature phase III migrating motor complex activity in the antrum, we investigated the effect of erythromycin on gallbladder volume in six patients with truncal vagotomy without gastric resection and 14 patients with antrectomy (6 with Billroth I anastomosis, 8 with Billroth II anastomosis), and we compared the results obtained with those in eight healthy controls. In addition, the effect of meal ingestion on gallbladder volume was studied. METHODS: Gallbladder volumes, measured with ultrasonography, were determined every 15 min for 180 min after erythromycin infusion (3 mg/kg i.v.), as well as 30 and 60 min after meal ingestion. RESULTS: Basal gallbladder volumes were not significantly different among the four groups. Erythromycin induced a significant (p < 0.01-0.05) gallbladder contraction of maximal 46 +/- 6% in the controls, 49 +/- 9% in the patients with truncal vagotomy, and 38 +/- 7% in the patients with antrectomy and Billroth I anastomosis. In the patients with antrectomy and Billroth II anastomosis, no significant reduction in gallbladder volume after erythromycin was observed. Meal-induced gallbladder contraction was normal in all patients, including those with Billroth II anastomosis. CONCLUSIONS: These results indicate that neither the long vagus nerve nor the antrum is essential for erythromycin-induced effects on the gallbladder. Because no significant reduction in gallbladder volume in response to erythromycin was observed in the patients with antrectomy and Billroth II anastomosis, we suggest that duodenojejunal anatomical integrity is essential for erythromycin-induced gallbladder contraction.

Adult↗
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

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

Effect of endoscopic sclerotherapy of esophageal varices on vagus nerve integrity.

Endoscopic sclerotherapy is an effective method of controlling variceal hemorrhage, but complications frequently occur. Recent studies have shown that sclerotherapy may induce transient alterations in gastrointestinal motility. It has been suggested that these complications result from vagal nerve injury due to sclerotherapy. We have tested this hypothesis by measuring pancreatic polypeptide secretion in response to insulin-induced hypoglycemia (insulin 0.1 U/kg i.v.), a well-known stimulus for vagal nerve function. We studied six patients with cirrhosis and variceal bleeding (group A, mean age 52 years) on two occasions, before and 3 days after the first sclerotherapy. In addition six other patients with cirrhosis (group B, mean age 51 years) 6 months after successful repeated sclerotherapy for esophageal varices and 12 control subjects (mean age 50 years) were investigated. Basal plasma pancreatic polypeptide concentrations were not significantly different between group A patients before sclerotherapy (28 +/- 4 pM) or after sclerotherapy (24 +/- 6 pM), group B patients (40 +/- 9 pM) and controls (29 +/- 4 pM). Although the plasma pancreatic polypeptide peak increment in response to insulin hypoglycemia was reduced in group A patients after sclerotherapy (90 +/- 35 pM) compared to pre-sclerotherapy (120 +/- 18 pM), to group B patients (146 +/- 20 pM) and to controls (143 +/- 7 pM), this difference was not significant. Nor did sclerotherapy significantly reduce the integrated pancreatic polypeptide secretion between or within groups. However, in two group A patients a transient and reversible reduction in pancreatic polypeptide secretion was observed directly after sclerotherapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Prospective evaluation of 24 hour ambulatory pH metry in Belsey Mark IV antireflux surgery.

This study evaluated the effect of the 270 degrees Belsey Mark IV fundoplication on 24 hour ambulatory pH metry variables. Thirty seven patients with confirmed gastro-oesophageal reflux disease who had a Belsey Mark IV antireflux procedure were evaluated preoperatively and three to six months postoperatively including endoscopy, lower oesophageal sphincter manometry, and 24 hour ambulatory pH metry. In 30 of 37 patients the Belsey Mark IV fundoplication was judged successful based on symptom relief and healing of oesophagitis. In these 30 patients percentage reflux for total, upright, and supine time (median and range) decreased significantly (p < 0.001) from 10.0% (2.7-35.3%), 10.8% (3.2-39.9%), and 6.7 (0.0-33.0%) respectively to 0.5% (0.0-7.4%), 0.6% (0.0-13.7%), and 0.1% (0.0-4.9%) after operation. This decrease in reflux time resulted predominantly from a significant (p < 0.001) reduction in the number of reflux episodes from 98 (23-231) to 14 (0-82) postoperatively. Normalisation of total reflux time (upper limit of normal for time with pH below 4:4%) was found in 89% and normalisation of total and upright and supine reflux in 64% of successfully operated patients with confirmed abnormal acid reflux before operation. A successful antireflux procedure was associated with significant (p < 0.001) increases in lower oesophageal sphincter pressure from 7.8 (0.6) mm Hg to 14.5 (0.7) mm Hg mean (SEM). In seven patients with a failed antireflux operation basal lower oesophageal sphincter pressure did not change significant;y (preoperative value 5.7 (1.3) mm Hg; postoperative value 7.8 (0.8) mm Hg). In these patients reflux time did not decrease after the operation and remained in the abnormal range in all patients. It is concluded that a successful, in contrast with a failed, Belsey Mark IV fundoplication is associated with significant decreases in total, upright, and supine reflux time. Normalisation of pH metry variables is not a prerequisite for successful antireflux surgery. A surgery. A successful 270 degree Belsey Mark IV fundoplication was associated with a significant increase in basal lower oesophageal sphincter pressure, in contrast with the failure group. Restoration of a sufficient lower oesophageal sphincter barrier is an important aim in antireflux surgery.

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

Significant satiety effect of bombesin in lean but not in obese subjects.

The aim of this work was to determine whether infusion of bombesin inhibits intake of a carbohydrate-rich meal in lean and obese women. A double blind study was carried out using bombesin or saline infusion. The subjects were nine lean and nine obese women of the same age. Food intake and hunger feelings were measured. During infusion of bombesin, the amount of food eaten by the lean individuals (294 +/- 55 g) was significantly less than during infusion of saline (467 +/- 69 g, P < 0.01). However, bombesin induced no significant feeding suppression in the obese women when compared to saline (431 +/- 60 vs 499 +/- 99 g). Subjective hunger feelings were significantly affected by bombesin infusion in the lean subjects only. It was concluded that bombesin infusion inhibits food intake and increases satiety in lean women, whereas obese women are less sensitive to these bombesin-induced satiety effects.

Adult↗
PubMed1994

Nutrient-specific effects of modified sham feeding on pancreatic polypeptide release.

OBJECTIVE: To study the effect of meal composition on pancreatic polypeptide release during modified sham feeding. DESIGN: In random order and on separate occasions, isocaloric, isothermic, isoosmotic, homogenized meals (1050 kJ; 250 kcal) either rich in fat (walnuts; 64 g fat, 7 g protein, 15 g starch per 100 g), protein (codfish, 1 g fat, 23 g protein per 100 g) or carbohydrates (bananas; 22 g starch, 1 g protein per 100 g) were sham-fed for 30 min by tasting and spitting out the meal. The plasma pancreatic polypeptide response was monitored by radioimmunoassay at 10 min intervals from 20 min before to 120 min after modified sham feeding. SETTING: Department of Gastroenterology and Hepatology of a University Hospital. SUBJECTS: Seven healthy volunteers: 3 male, 4 female; age 45 (range 30-77) years. RESULTS: Integrated plasma pancreatic polypeptide responses to modified sham feeding of codfish (1088 +/- 395 pM*120 min; P < 0.05) and walnuts (1200 +/- 542 pM*120 min) were distinctly higher (P < 0.05) than to modified sham feeding of bananas (-390 +/- 291 pM*120 min). CONCLUSIONS: These results demonstrate that the pancreatic polypeptide response to modified sham feeding is dependent on the composition of the meal.

Adult↗
PubMed1994

Plasma cholecystokinin and pancreatic polypeptide secretion in response to bombesin, meal ingestion and modified sham feeding in lean and obese persons.

Disturbed satiety mechanisms may contribute to obesity. There has been speculation that cholecystokinin (CCK) and pancreatic polypeptide (PP) are involved in the regulation of satiety. We have therefore investigated whether there are differences between healthy lean and healthy non-diabetic obese volunteers in plasma CCK or PP release after a neuropeptidergic stimulation with bombesin and after infusion of a mixed meal. There were no differences in plasma CCK between groups either basally or in response to either form of stimulation. However, the plasma PP concentrations after the meal were significantly less in obese (2845 +/- 404 pM.min) than in lean subjects (5569 +/- 997 pM.min), whereas the plasma PP concentrations during bombesin were similar in both groups. We tested two other groups of nine obese and lean subjects to determine whether a disturbed vagal function could be the cause of the diminished plasma PP in obese persons, by studying the effect of modified sham feeding (MSF) on plasma PP. However, there were no significant differences in the plasma PP response to MSF between lean and obese subjects. We conclude that there are no differences between lean and obese persons in plasma CCK secretion in response to infusion of the neuropeptide bombesin or to ingestion of a mixed meal. However, the plasma PP after a mixed meal, is markedly diminished in obese subjects. This could not be attributed to a disturbed vagal cephalic stimulation.

Adult↗
PubMed1993

Effects of a physiological dose of cholecystokinin on food intake and postprandial satiation in man.

CCK-33 was infused intravenously to groups of 9 lean and 9 obese volunteers in doses that elicited plasma CCK concentrations in the physiological range. The effect of these infusions on food intake and satiety signals was compared with the effect of saline infusions in the same subjects. Food intake (486 +/- 52 g; mean +/- S.E.M.) was slightly, but not significantly decreased (553 +/- 55 g after saline), and hunger and fullness feelings after eating were unaffected, in both of the two groups. We conclude that the infusion of CCK-33 to plasma levels comparable to those observed after a fatty meal does not have a major effect on food intake and postprandial hunger feelings.

Adult↗
PubMed1993

Effect of cholestyramine and cholecystokinin receptor antagonist CR1505 (loxiglumide) on lower esophageal sphincter pressure in man.

Cholecystokinin (CCK) decreases lower esophageal sphincter pressure (LESP) in man. Cholestyramine, a nonabsorbable bile salt binding resin, stimulates endogenous CCK secretion. We have investigated the effect of oral ingestion of 16 g cholestyramine without and with infusion of the CCK receptor antagonist CR1505 (loxiglumide, 15 mg/kg/90 min) on LESP in seven healthy subjects. LESP was recorded for 90 min, in 10-min intervals, with the pull-through technique using a four-lumen water-perfused catheter. Oral ingestion of cholestyramine resulted in a significant (P < 0.05) decrease in LESP, starting from 10 min and continuing during the entire experiment (basal LESP: 11.8 +/- 2 mm Hg, minimal value reached during cholestyramine: 7.3 +/- 1 mm Hg; P < 0.05). Pretreatment with loxiglumide completely antagonized the effect of cholestyramine on LESP. Infusion of loxiglumide without cholestyramine did not affect basal LESP. It is concluded that: (1) cholestyramine significantly reduces LESP; (2) this reduction in LESP does not occur after pretreatment with loxiglumide, indicating that cholestyramine influences LESP through CCK release; and (3) basal LESP is not regulated by CCK.

Adult↗
PubMed1993

Hyperglycemia modulates gallbladder motility and small intestinal transit time in man.

The aim of the present study was to investigate the effect of acute hyperglycemia on (1) the intestinal phase of gallbladder contraction induced by the intraduodenal administration of emulsified fat, and (2) the small intestinal transit time measured by the lactulose breath hydrogen test. Six healthy volunteers were studied in random order during normoglycemia and hyperglycemia (blood glucose levels 15 mmol/liter). Gallbladder volumes were measured with ultrasonography. Administration of 1 and 2 g/hr of fat resulted in significant reductions in gallbladder volumes from 24 +/- 2 cm3 to 11 +/- 1 cm3 (P < 0.05) and 8 +/- 1 cm3 (P < 0.05), respectively during normoglycemia, and from 24 +/- 2 cm3 to 21 +/- 2 cm3 (P < 0.05) and 16 +/- 2 cm3, respectively (P < 0.05) during hyperglycemia. Compared to normoglycemia, the gallbladder contraction was significantly (P < 0.05) reduced during hyperglycemia. No significant differences in CCK secretion were observed between experiments. Small intestinal transit time during hyperglycemia (101 +/- 12 min) was significantly (P < 0.05) prolonged compared to normoglycemia (57 +/- 12 min). During hyperglycemia, basal PP levels and PP secretion in response to intraduodenal fat were significantly (P < 0.05) reduced compared to normoglycemia. It is concluded that (1) low doses of intraduodenal emulsified fat result in significant gallbladder contraction and CCK secretion, (2) acute hyperglycemia inhibits intraduodenal fat induced gallbladder contraction, (3) acute hyperglycemia does not affect the intraduodenal fat induced CCK secretion, (4) small intestinal transit is significantly prolonged during acute hyperglycemia, and (5) acute hyperglycemia inhibits basal and stimulated plasma PP secretion, suggesting impaired vagal-cholinergic tone during hyperglycemia.

Acute Disease↗
PubMed1993

Hyperglycemia reduces gallbladder emptying and plasma hormone secretion to modified sham feeding and regular feeding.

The purpose of this study was to investigate the effect of acute stable hyperglycemia on gallbladder motility, plasma cholecystokinin level and pancreatic polypeptide secretion. Gallbladder emptying in response to modified sham feeding and regular feeding was determined in six healthy subjects on two separate occasions during normoglycemia (serum glucose = 5 mmol/L) and during hyperglycemia (serum glucose = 15 mmol/L). Pancreatic polypeptide secretion was determined as an indirect measure of cholinergic tone. Gallbladder contraction in response to sham feeding during hyperglycemia (9% +/- 2%) was significantly (p < 0.05) reduced compared with that in normoglycemia (22% +/- 1%). During hyperglycemia, gallbladder emptying after meal ingestion (29% +/- 9%) was significantly (p < 0.05) less than that in normoglycemia (60% +/- 10%). Sham feeding did not affect plasma cholecystokinin levels. Regular feeding induced significant (p < 0.05) increases in plasma cholecystokinin levels in both experiments. However, integrated postprandial plasma cholecystokinin secretion was significantly (p < 0.05) reduced during hyperglycemia compared with that in normoglycemia (29 +/- 5 pmol.60 min vs. 58 +/- 10 pmol.60 min). Modified sham feeding-and feeding-stimulated pancreatic polypeptide secretion during hyperglycemia (235 +/- 95 pmol.90 min and 1,035 +/- 267 pmol.60 min, respectively) were significantly (p < 0.05) less than levels seen in normoglycemia (434 +/- 71 pmol.90 min and 1,961 +/- 219 pmol.60 min, respectively). This study indicates that gallbladder emptying and plasma hormone secretion in response to sham feeding and regular feeding are affected by blood glucose levels.

Adult↗
PubMed1993

Bombesin reduces food intake after a preload in man by a cholecystokinin-independent mechanism.

1. A double-blind study was undertaken to determine whether the infusion of bombesin inhibits the intake of a carbohydrate-rich meal, consumed 15 min after a 300 ml banana shake, in nine lean healthy subjects and whether the possible inhibition of food intake by bombesin is mediated by cholecystokinin. 2. The amount of food eaten during infusion of bombesin (267 +/- 60 g) and bombesin combined with the cholecystokinin-receptor antagonist loxiglumide (269 +/- 39 g) was slightly (P = 0.09) less than during saline infusion (384 +/- 40 g). In addition, preprandial feelings of hunger were significantly less during infusion of both bombesin and bombesin combined with loxiglumide. 3. In conclusion, infusion of bombesin tends to inhibit the intake of a carbohydrate-rich meal after a preload by a cholecystokinin-independent mechanism.

Adult↗
PubMed1993

Effect of acute hyperglycaemia on gall bladder contraction induced by cholecystokinin in humans.

This study examined the effect of acute hyperglycaemia, induced by intravenous glucose, on gall bladder motility. Six healthy volunteers were studied in random order on three occasions during normoglycaemia and hyperglycaemia with blood glucose concentrations stabilised at 8 and 15 mmol/l. Gall bladder volumes, measured with ultrasonography, were studied before and during infusion of stepwise increasing doses of cholecystokinin (CCK-33; 0.25, 0.5, and 1.0 IDU.kg-1.h-1). Each dose was given for 30 minutes. Pancreatic polypeptide (PP) secretion was determined as an indirect measure of cholinergic tone. Infusion of CCK-33 resulted in significant dose dependent reductions in gall bladder volume in all three experiments. Compared with normoglycaemia the gall bladder contraction was significantly (p < 0.05) reduced during infusion of 0.25 and 0.5 IDU kg-1.h-1 CCK-33 in the 8 mmol/l hyperglycaemic experiment, and during infusion of 0.25, 0.5, and 1.0 IDU kg-1.h-1 CCK-33 in the 15 mmol hyperglycaemic experiment. During hyperglycaemia basal plasma PP concentrations and PP secretion in response to CCK-33 were significantly (p < 0.05) reduced. It is concluded that blood glucose concentrations affect gall bladder motility, that an acute hyperglycaemia at 8 and 15 mmol/l reduces the gall bladder responsiveness to CCK-33 in a dose dependent manner, and that hyperglycaemia reduces basal and CCK-33 stimulated plasma PP concentrations, suggesting impaired cholinergic activity during hyperglycaemia.

Adult↗
PubMed1993

Hyperglycemia reduces gastric secretory and plasma pancreatic polypeptide responses to modified sham feeding in humans.

We have investigated the effect of acute stable hyperglycemia on gastric acid secretion and serum gastrin and pancreatic polypeptide (PP) release. Gastric acid output was measured under basal conditions and in response to modified sham feeding (MSF) in 7 healthy volunteers on two separate occasions: during normoglycemia (serum glucose 5 mmol/l) and during hyperglycemia (serum glucose 15 mmol/l). PP secretion was determined as an indirect measure of vagal-cholinergic tone. Basal acid output during hyperglycemia (4.7 +/- 1.0 mmol/h) was not significantly different from euglycemia (5.4 +/- 0.6 mmol/h), but MSF-stimulated acid output during hyperglycemia (14.7 +/- 3.3 mmol/90 min) was significantly (p < 0.05) reduced compared to euglycemia (24.7 +/- 3.2 mmol/90 min). Serum gastrin levels were not affected by MSF. During hyperglycemia, the integrated PP secretion in response to MSF (235 +/- 95 pmol/l.90 min) was significantly (p < 0.05) reduced compared to euglycemia (434 +/- 71 pmol/l.90 min). This study indicates that (1) serum glucose affects cephalic-stimulated gastric acid secretion, and (2) PP secretion after MSF is significantly reduced during hyperglycemia suggesting impaired vagal-cholinergic activity during hyperglycemia.

Adult↗