Biomedical subjects

A A Masclee

Publications and source records attributed to A A Masclee.

At least 19 recordsLinked to original sources

PubMed1999

Effect of acute hyperglycemia on basal, secretin and secretin + cholecystokinin stimulated exocrine pancreatic secretion in humans.

Pancreatico-biliary secretion is reduced during acute hyperglycemia. We investigated whether alterations in pancreatico-biliary flow or volume output are responsible for the observed reduction in duodenal output of pancreatic enzymes and bilirubin during hyperglycemia. Eight healthy subjects were studied on two occasions during normoglycemia and hyperglycemia (15 mmol/l). Pancreatico-biliary output was measured by aspiration using a recovery marker under basal conditions (60 min), during secretin infusion (0.1 CU/kg.h) for 60 min and during secretin + CCK (0.5 IDU/kg.h) infusion for 60 min. Secretin was infused to stimulate pancreatico-biliary flow and volume output. Secretin significantly (P<0.005-P<0.05) increased volume and bicarbonate output and CCK significantly (P<0.01) increased the output of bilirubin, pancreatic enzymes, bicarbonate and volume, both during normoglycemia and hyperglycemia. During hyperglycemia basal, secretin stimulated and secretin + CCK stimulated total pancreatico-biliary output were significantly (P<0.005-P<0.05) reduced compared to normoglycemia. The incremental outputs, however, were not significantly different between hyper- and normoglycemia. Pancreatic volume output was significantly (P<0.05) reduced during hyperglycemia compared to normoglycemia under basal conditions (31+/-16 m/h versus 132+/-33 m/h) during secretin infusion (130+/-17 ml/h versus 200+/-34 m/h) and during secretin + CCK infusion (370+/-39 ml/h versus 573+/-82 ml/h). Plasma PP levels were significantly (P<0.05) reduced during hyperglycemia. It is concluded that 1) hyperglycemia significantly reduces basal pancreatico-biliary output 2) the incremental pancreaticobiliary output in response to secretin or secretin + CCK infusion is not significantly affected during hyperglycemia, 3) a reduction in volume output contributes to the inhibitory effect of hyperglycemia on pancreatico-biliary secretion, 4) hyperglycemia reduces PP secretion suggesting vagal-cholinergic inhibition of pancreatico-biliary secretion and volume during hyperglycemia.

Adult↗

PubMed1999

Effect of intravenous amino acids on interdigestive antroduodenal motility and small bowel transit time.

BACKGROUND: Patients on total parenteral nutrition have an increased risk of developing gallstones because of gall bladder hypomotility. High dose amino acids may prevent biliary stasis by stimulating gall bladder emptying. AIMS: To investigate whether intravenous amino acids also influence antroduodenal motility. METHODS: Eight healthy volunteers received, on three separate occasions, intravenous saline (control), low dose amino acids (LDA), or high dose amino acids (HDA). Antroduodenal motility was recorded by perfusion manometry and duodenocaecal transit time (DCTT) using the lactulose breath hydrogen test. RESULTS: DCTT was significantly prolonged during LDA and HDA treatment compared with control. The interdigestive motor pattern was maintained and migrating motor complex (MMC) cycle length was significantly reduced during HDA compared with control and LDA due to a significant reduction in phase II duration. Significantly fewer phase IIIs originated in the gastric antrum during LDA and HDA compared with control. Duodenal phase II motility index was significantly reduced during HDA, but not during LDA, compared with control. CONCLUSIONS: Separate intravenous infusion of high doses of amino acids in healthy volunteers: (1) modulates interdigestive antroduodenal motility; (2) shortens MMC cycle length due to a reduced duration of phase II with a lower contractile incidence both in the antrum and duodenum (phase I remains unchanged whereas the effect on phase III is diverse: in the antrum phase III is suppressed and in the duodenum the frequency is increased); and (3) prolongs interdigestive DCTT.

Adult↗

PubMed1998

Influence of hyperglycemia on the satiating effect of CCK in humans.

In the present study the effects of intraduodenal (i.d.) fat (endogenous CCK) and of CCK infusion on satiety were studied during normo-and hyperglycemic conditions. Eight healthy subjects participated in two protocols consisting of two experiments each. First protocol: (a) normoglycemia (control) with i.d. emulsified fat (i.d. fat) infusion, (b) acute hyperglycemia (HG) with plasma glucose levels stabilized at 15 mmol/L and i.d. fat infusion. In the second protocol the effect of exogenous cholecystokinin (CCK) on satiety was studied during normo- and hyperglycemia. Intraduodenal fat (Intralipid 10%) was infused at a dose of 1 g/h via a nasoduodenal tube in the first protocol, whereas in the second protocol CCK-33 was infused intravenously at a dose of 0.5 IDU/kg x h. Satiety was scored using visual analog scales (VAS). Plasma CCK levels were determined at regular intervals. During infusion of i.d. fat and i.v. CCK the VAS scores of wish to eat, hunger, and prospective feeding decreased significantly (p<0.05) in the normoglycemic experiments. During hyperglycemia satiety did not significantly change in the basal period; however, the scores of wish to eat, hunger, and prospective feeding increased significantly (p<0.05) when i.d. fat or i.v. CCK was administered. Plasma CCK levels in the basal and the stimulated period were not significantly different between normo- and hyperglycemia. In summary, the present study shows that in healthy humans volunteers 1) during normoglycemic conditions satiety can be induced by very low dose of i.d. fat and by CCK infusion, 2) during hyperglycemia the effect of i.d. fat and CCK on satiety are reversed, resulting in increased appetite.

Adult↗

PubMed1998

Effects of hyperglycemia and hyperinsulinemia on satiety in humans.

Hyperglycemia may influence satiety. One mechanism by which glucose could influence food intake is hyperinsulinemia. Therefore, we investigated the short-term effects of acute hyperglycemia and euglycemic hyperinsulinemia on satiety. Six healthy volunteers (aged 20 to 26 years) were studied for 240 minutes on three separate occasions in random order during (1) intravenous (i.v.) saline (control), (2) acute hyperglycemic hyperinsulinemia (HG) with plasma glucose at 15 mmol/L, and (3) euglycemic hyperinsulinemia (HI) with plasma insulin at 80 mU/L and glucose at 4 to 5 mmol/L. Subjective criteria for appetite like the wish to eat, prospective feeding intentions ("How much food do you think you can eat?"), and feelings of hunger and fullness were scored on a 100-mm visual analog scale (VAS) at 30-minute intervals. Appetite was also measured every 60 minutes with the use of a food selection list (FSL). Appetite (prospective feeding intentions, feelings of hunger, and the wish to eat) gradually increased over basal levels during control conditions and HI. In contrast, prospective feeding intentions and feelings of hunger gradually decreased during HG and were significantly (P < .05) reduced versus basal and control levels during the last hour of the experiment. The wish to eat followed the same pattern. Feelings of fullness did not significantly change in all three experiments. Total food selection was not significantly decreased during HG, but the preference for fat-rich or carbohydrate-rich items tended to be reduced. The study suggests that in humans hyperglycemia induces satiety. This effect seems not to be mediated by insulin, since HI had no effect on appetite. However, a potentiating effect of endogenous insulin on the satiating effect of high blood glucose levels cannot be excluded.

Adult↗

PubMed1998

Effect of insulin on basal and cholecystokinin-stimulated gallbladder motility in humans.

BACKGROUND/AIMS: Acute hyperglycemia inhibits gallbladder contraction. In non-diabetic subjects this inhibitory effect may result from endogenous hyperinsulinemia. Therefore we investigated the effects of acute hyperglycemia and euglycemic hyperinsulinemia on basal and cholecystokinin-stimulated gallbladder motility. METHODS: Gallbladder volume (ultrasonography) and duodenal bilirubin output were studied simultaneously in nine healthy volunteers (age 20-52 years) on 3 separate occasions in random order during: (a) saline infusion (control), (b) hyperglycemic hyperinsulinemic clamping (HG; plasma glucose at 15 mmol/l), and (c) euglycemic hyperinsulinemic clamping (HI; plasma insulin at 150 mU/l, glucose at 4-5 mmol/l). After a 2-h basal clamp period, cholecystokinin was infused intravenously for 60 min at 0.25 IDU x kg(-1) x h(-1), followed by another 60 min at 0.5 IDU x kg(-1) x h(-1). RESULTS: HI and HG significantly (p<0.05) reduced basal duodenal bilirubin output compared to control, while basal gallbladder volume did not change. At the low dose cholecystokinin, gallbladder emptying during HG (25+/-3%) and HI (39+/-4%) was significantly (p<0.01) reduced compared to control (61+/-4%). The inhibitory effect of HG was significantly (p<0.05) stronger compared to HI. Duodenal bilirubin output during the low dose cholecystokinin was significantly (p<0.05) reduced by HG, but not by HI. No inhibitory effect of HG and HI on gallbladder emptying and duodenal bilirubin output was observed with the high dose of cholecystokinin. CONCLUSIONS: In healthy subjects acute hyperglycemia and euglycemic hyperinsulinemia reduce basal duodenal bilirubin output and inhibit gallbladder emptying stimulated by low dose cholecystokinin. These results suggest that insulin is involved in the inhibitory effect of hyperglycemia on basal and cholecystokinin-stimulated gallbladder motility.

Adult↗

PubMed1998

Effect of amino acids on lower esophageal sphincter characteristics and gastroesophageal reflux in humans.

The effect of a commercially available mixed amino acids solution, when given either intravenously or intragastrically, on lower esophageal sphincter (LES) pressure, frequency of transient LES relaxations (TLESRs) and gastroesophageal reflux (GER) was investigated in six healthy volunteers. LES pressure and esophageal pH were simultaneously recorded on three separate occasions 1 hr before (basal) and 3 hr during intravenous or intragastric infusion of amino acids (250 mg protein/kg/hr) or saline (control). No significant changes in LES pressure were seen in the control experiment. Intravenous amino acids caused a rapid and sustained (P < 0.01) decrease in LES pressure whereas intragastric amino acids decreased LES pressure only gradually and temporarily (P < 0.01). In the three experiments no significant differences were observed in TLESR frequency, the number of GER episodes, the mechanism of reflux, or duration of acid exposure. In healthy subjects both intragastric and, especially, intravenous infusion of amino acids significantly decrease LES pressure but do not affect the frequency of TLESRs or GER episodes during a continuous liquid gastric load.

Adult↗

PubMed1998

Obese women are less sensitive for the satiety effects of bombesin than lean women.

OBJECTIVE: The aim of this study was to investigate whether infusion of bombesin, when combined with a gastric preload, influence satiety and foot intake in obese and lean healthy women. DESIGN: Double blind, placebo controlled study. SETTING: Department of Gastroenterology, Leiden University Medical Center, The Netherlands. SUBJECTS: Obese (n = 7) and lean (n = 7) healthy women. INTERVENTIONS: Intravenous infusion of bombesin (0.09 nmol/kg ideal weight/h) or placebo for 165 min. Gastric preload of banana slices was administered at time 60 min. Meal ingestion started at time 75 min (banana slices). Food intake was calculated and satiety was measured by visual analog scales. RESULTS: During infusion of bombesin the amount of food eaten by the lean individuals (193+/-37 g) was significantly reduced compared to saline infusion (365+/-42 g, P < 0.05). However, bombesin induced no significant feeding suppression in obese women when compared to saline (241+/-46 vs 301+/-45 g, respectively). The decrease in food intake during bombesin infusion compared to saline was significantly greater in lean subjects (173+/-30 g) than in obese subjects (59+/-35 g; P < 0.05). Only in lean subjects subjective preprandial hunger feelings were significantly affected by bombesin infusion. CONCLUSIONS: Infusion of bombesin, when combined with a gastric preload, inhibits food intake and increases satiety in lean women. Obese women are less sensitive for these bombesin induced satiety effects.

Adult↗

PubMed1998

Interdigestive antroduodenal motility and gastric acid secretion.

BACKGROUND: In humans, interdigestive acid secretion and antroduodenal motility are closely related with cyclic variations in acid secretion, synchronous with the various phases of the migrating motor complex (MMC). Duodenal acidification inhibits antral motility, but little is known about the effect of acute acid inhibition on antroduodenal motility. AIM: To study the effect of acute acid inhibition on antroduodenal motility. SUBJECTS: Ten healthy volunteers (four men and six women: age range 20-31 years). METHODS: Antroduodenal motility (perfusion manometry) and gastric acid secretion (continuous aspiration with recovery marker) were measured simultaneously. Each subject was studied twice in random order during (1) intravenous infusion of saline for one-two complete MMC cycles and (2) during acute acid inhibition with intravenous famotidine (bolus 20 mg, continuous infusion 4 mg/h) for one-two complete MMC cycles or at least 240 min. RESULTS: In the saline study, acid output in phase III (2.1 +/- 0.3 mmol/10 min) and late phase II (1.7 +/- 0.2 mmol/10 min) was significantly (P<0.05) increased over early phase II and phase I (1.2 +/- 0.2 and 1.2 +/- 0.2 mmol/10 min, respectively). Famotidine increased gastric pH to above pH 6 within 30 min. After acid inhibition, duration of MMC cycle during famotidine (106 +/- 8 min) was not significantly different from the saline experiment (133 +/- 14 min). Phase distribution of the MMC cycle was not significantly different between famotidine (I, II and III: 12 +/- 3, 82 +/- 3 and 5 +/- 1%) and saline (I, II and III: 13 +/- 3, 83 +/- 3 and 4 +/- 1%). CONCLUSIONS: Gastric acid secretion varies cyclically with interdigestive antroduodenal motility. Acute acid inhibition with intravenous famotidine does not significantly affect interdigestive antroduodenal motility.

Adult↗

PubMed1998

Effects of somatostatin on proximal gastric motor function and visceral perception.

BACKGROUND: Somatostatin affects gastrointestinal motility and secretion and visceral sensation, but little is known about its effects on the proximal stomach. AIM: To evaluate the effects of somatostatin on proximal gastric motor function and perception of symptoms. METHODS: Six healthy subjects participated in two experiments performed in random order during continuous intravenous infusion of saline or somatostatin (250 microg/h). Proximal gastric motor function was evaluated using a barostat. We performed pressure and volume distensions and a barostat procedure (minimal distending pressure + 2 mmHg). Symptoms were evaluated at regular intervals using visual analogue scales (VAS). RESULTS: Neither minimal distending pressure nor gastric fundal tone were significantly different between somatostatin and saline. Pressure-volume curves during distensions were not influenced by somatostatin. However, phasic volume waves were significantly (P < 0.001) reduced by somatostatin, and somatostatin significantly (P < 0.05) reduced symptom perception of fullness and abdominal pressure during stepwise distensions.

Adult↗

PubMed1998

Hyperglycaemia reduces gastrin-stimulated gastric acid secretion in humans.

BACKGROUND: Recent studies have pointed to the role of plasma glucose in the regulation of gastrointestinal function. METHODS: We have investigated the effect of acute hyperglycaemia on gastric acid secretion and pancreatic polypeptide (PP) release. Gastric acid output was measured under basal conditions and in response to intravenous infusion of gastrin-17 in two doses: 5 pmol kg-1 h for 60 min and 15 pmol kg-1 h for another 60 min. Seven healthy subjects were studied during normoglycaemia and during acute hyperglycaemia at 15 mmol L-1. Acid output was measured by continuous aspiration using phenol red as recovery marker. Plasma PP levels were determined at regular intervals. RESULTS: Gastrin infusion at 5 pmol kg-1 h significantly (P < 0.05) increased acid output both during normoglycaemia and during hyperglycaemia. Gastrin infusion at 15 pmol kg-1 h further and significantly (P < 0.05) increased the acid output during both experiments. Hyperglycaemia significantly (P < 0. 05) reduced basal acid output (2.5 +/- 0.9 vs. 6.3 +/- 1.9 mmol h-1), low-dose gastrin stimulated acid output (6.5 +/- 1.7 vs. 13.0 +/- 1. 8 mmol h-1) and high-dose gastrin stimulated acid output (11.7 +/- 3. 0 vs. 19.4 +/- 3.0 mmol h-1) compared with normoglycaemia. Plasma PP levels were not stimulated by gastrin-17 infusion and were significantly (P < 0.05) reduced during hyperglycaemia. CONCLUSIONS: (a) Basal and gastrin-17-stimulated gastric acid secretion are reduced during hyperglycaemia; (b) infusion of gastrin-17 to physiological post-prandial levels does not affect plasma PP levels; (c) plasma PP levels are reduced during hyperglycaemia, suggesting vagal-cholinergic inhibition of gastric acid secretion during hyperglycaemia.

Adult↗

PubMed1998

Dose-dependent inhibition of postprandial gallbladder motility and plasma hormone secretion during acute hyperglycemia.

BACKGROUND: Actual blood glucose concentrations influence gastrointestinal function. We investigated whether in healthy subjects the inhibitory effect of acute hyperglycemia on gallbladder motility is dose-dependent. METHODS: Seven healthy volunteers were studied on four separate occasions in random order during euglycemia and during hyperglycemic clamping, at 4 mmol/l, 8 mmol/l, 12 mmol/l, and 16 mmol/l, respectively. Gallbladder volumes (ultrasonography) and plasma hormone release were studied before and after ingestion of a meal. RESULTS: Postprandial gallbladder contraction was significantly (P < 0.05) and dose-dependently inhibited during the hyperglycemic experiments at 8, 12, and 16 mmol/l (56%+/-8%, 49%+/-8%, and 30%+/-5%, respectively) compared with euglycemia (68%+/-6%). Postprandial cholecystokinin release was significantly (P < 0.05) reduced compared with euglycemia only at a plasma glucose level of 16 mmol/l (116+/-28 versus 159+/-13 pmol x l(-1) x 120 min). Plasma pancreatic polypeptide secretion, as an indirect measure of vagal-cholinergic tone, was significantly (P < 0.05) and dose-dependently reduced during hyperglycemia at 8, 12, and 16 mmol/l. CONCLUSION: In healthy subjects acute hyperglycemia significantly and dose-dependently inhibits postprandial gallbladder motility. Future studies on gallbladder motility should take into account the influence of plasma glucose, because already at postprandial glucose levels gallbladder motility is reduced.

Adult↗

PubMed1998

Prospective study of the effect of the Belsey Mark-IV fundoplication on reflux mechanisms.

BACKGROUND: Transient lower esophageal sphincter relaxations (TLESRs) are the major mechanism permitting gastroesophageal reflux (GER). Little information is available on how anti-reflux surgery affects reflux mechanisms, especially TLESRs. We evaluated the effects of partial fundoplication (Belsey Mark IV) on reflux mechanisms. METHODS: Sixteen patients were prospectively studied before and after Belsey Mark-IV operation by endoscopy, 24-h esophageal pH-metry, and simultaneous recording of pH and lower esophageal sphincter (LES) characteristics by sleeve manometry. RESULTS: The operation was successful in 14 of 16 patients (87%). Fasting and postprandial reflux decreased significantly (P < 0.01) after the operation. Partial fundoplication significantly (P < 0.05) decreased the number of TLESRs per hour in the fasting and postprandial period from 3.2+/-0.4 and 5.6+/-0.5 to 1.7+/-0.3 and 2.8+/-0.4, respectively. The percentage of TLESRs associated with reflux also decreased significantly (P < 0.05). Basal LES pressure increased from 14.7+/-2.1 mmHg to 17.9+/-2.6 mmHg (not significant). CONCLUSIONS: Partial fundoplication controls GER through a reduction in the number of TLESRs and by decreasing the number of relaxations associated with reflux.

Adult↗

PubMed1998

Effect of acute hyperglycemia on basal and bombesin-stimulated pancreaticobiliary secretion in humans.

This study was undertaken to investigate the effect of acute hyperglycemia on basal and bombesin-stimulated pancreaticobiliary secretion. Seven healthy subjects participated in two experiments performed in random order during normoglycemia and hyperglycemic clamping at 15 mM. Duodenal outputs of bilirubin, trypsin, amylase, and bicarbonate were measured by aspiration with a recovery marker under basal conditions for 60 min and during continuous infusion of bombesin (1 ng/kg x min) for 60 min. Plasma cholecystokinin (CCK) and pancreatic polypeptide (PP) levels were determined at regular intervals. Compared to normoglycemia, during hyperglycemia basal outputs of bilirubin (17 +/- 3 vs. 0.9 +/- 0.4 micromol/60 min), trypsin (24 +/- 4 vs. 4 +/- 1 U/60 min), amylase (12 +/- 1 vs. 3 +/- 1 kU/60 min), and bicarbonate (2.9 +/- 0.5 vs. 1.2 +/- 0.2 mmol/60 min) were significantly p < 0.05) reduced. Bombesin significantly (p < 0.05) increased pancreaticobiliary output during both normo- and hyperglycemia. During hyperglycemia bombesin-stimulated 60-min outputs of bilirubin, trypsin, amylase, and bicarbonate were not significantly different compared to those during normoglycemia. Basal and bombesin-stimulated plasma PP concentrations were significantly (p < 0.05) reduced during hyperglycemia, but plasma CCK levels were not significantly different. It is concluded that acute hyperglycemia reduces basal but does not affect bombesin-induced pancreaticobiliary secretion.

Acute Disease↗

PubMed1998

Is Barrett's esophagus characterized by more pronounced acid reflux than severe esophagitis?

OBJECTIVE: Barrett's esophagus is related to gastroesophageal reflux disease (GERD). However, only a small fraction of patients with GERD develop Barrett's esophagus. We evaluated whether gastroesophageal acid reflux is more pronounced in Barrett's patients than in patients with moderate or severe endoscopic esophagitis. METHODS: Retrospective evaluation of results of esophageal manometry and 24 hour ambulatory pH monitoring performed between 1990 and 1996 at the Leiden University Medical Center in those patients who also underwent endoscopy < or = 3 months before pH-metry. Included were 51 patients with Barrett's esophagus, 30 patients with severe esophagitis, 45 patients with moderate esophagitis, and 24 healthy control subjects. RESULTS: Patients with Barrett's esophagus had significantly increased acid reflux time (p < 0.01-0.05) compared to patients with moderate, but not compared to patients with severe esophagitis. Distal esophageal body motility and LES pressure were significantly (p < 0.01-0.05) reduced in patients with Barrett's esophagus compared to patients with moderate esophagitis but not compared to those with severe esophagitis. CONCLUSION: Although acid reflux is increased in patients with Barrett's esophagus and esophageal motility is impaired, other factors apart from acid exposure and motility contribute to the development of Barrett's esophagus.

Analysis of Variance↗

PubMed1998

Effect of intragastric or intraduodenal administration of a polymeric diet on gallbladder motility, small-bowel transit time, and hormone release.

OBJECTIVE: During postpyloric tube feeding, GI intolerance is observed more frequently than during prepyloric feeding, possibly by evoking a stronger GI response. METHODS: We investigated the effect of intragastric and intraduodenal administration of a polymeric diet (125 kcal/h) on gallbladder motility (by ultrasonography), duodeno-cecal transit time (by lactulose H2 breath test), and GI hormone release (including cholecystokinin, pancreatic polypeptide, and gastrin). Six healthy subjects (two male, four female; mean age 22 yr, range 18-27 yr) were studied on two separate occasions in random order during 6 h of continuous administration of the diet through either the gastric or duodenal port of a two-lumen tube. RESULTS: Intraduodenal feeding resulted in a more rapid contraction of the gallbladder, from 32 +/- 4 to 23 +/- 4 cm3 at 10 min (p < 0.05), reaching a minimum of 6 +/- 1 cm3, in contrast to intragastric feeding (31 +/- 4 to 19 +/- 3 cm3 at 60 min, p < 0.05; minimum 14 +/- 1 cm3). The gallbladder remained contracted during the 6-h study period during both intraduodenal and intragastric feeding. Small-bowel transit time was significantly accelerated during intraduodenal compared with intragastric feeding (51 +/- 12 vs 81 +/- 9 min; p = 0.003). Plasma cholecystokinin secretion was significantly (p < 0.05) increased during intraduodenal compared with intragastric feeding (848 +/- 107 vs 279 +/- 89 pmol x L(-1) x 360 min). The same was true for pancreatic polypeptide secretion. However, gastrin release was significantly (p < 0.05) higher during intragastric feeding. CONCLUSIONS: Intraduodenal feeding elicited a stronger GI response than intragastric feeding, as demonstrated by accelerated small-bowel transit time, more rapid and stronger gallbladder contractions, and increased cholecystokinin and pancreatic polypeptide release. Gastrin release, on the other hand, was stronger during intragastric feeding.

Adolescent↗

PubMed1998

Measurement of superior mesenteric artery flow by means of Doppler ultrasound in early dumping syndrome.

OBJECTIVE: Dumping occurs in about 10% of patients after gastric surgery. It has been suggested that early dumping is associated with an abnormal increase in postprandial splanchnic flow, but data from controlled studies are lacking. Therefore we have studied basal and postprandial superior mesenteric artery (SMA) blood flow in patients with dumping and in two control groups. METHODS: Three groups were studied, one group of patients after gastric surgery with early dumping (n = 6), one surgical control group with patients after gastric surgery without dumping symptoms (n = 7), and a healthy control group without previous gastric surgery (n = 10). Blood glucose and heart rate were measured after dumping provocation by oral ingestion of 50 g glucose. SMA blood flow was measured both basally and 20 min after glucose ingestion. RESULTS: Basal SMA flow was similar in the three groups. After glucose ingestion SMA flow was not significantly different between dumping patients and surgical controls. However, stimulated SMA flow in both groups after gastric surgery combined was significantly (p < 0.05) higher than in healthy controls. CONCLUSION: The systemic symptoms associated with early dumping do not result from increased SMA blood flow per se. After gastric surgery patients have an increased postprandial SMA flow irrespective of the presence of dumping.

Adult↗

PubMed1998

Effect of CCK on proximal gastric motor function in humans.

We have studied the effect of CCK on proximal gastric motor function in humans. Seven healthy volunteers participated in three experiments performed in random order during continuous intravenous infusion of 1) saline (control), 2) 0.5 IDU.kg-1.h-1 CCK, and 3) 1.0 IDU.kg-1.h-1 CCK. Proximal gastric mechanics were measured by an electronic barostat, and abdominal symptoms were scored by visual analog scales. Infusion of 0.5 and 1.0 IDU.kg-1.h-1 CCK resulted in plasma CCK levels (RIA) in the postprandial range. CCK induced gastric relaxation; at 2 mmHg above intra-abdominal pressure the intragastric volume during 1.0 IDU.kg-1.h-1 CCK was significantly increased over saline (363 +/- 44 vs. 195 +/- 34 ml; P < 0.01) but not during 0.5 IDU.kg-1.h-1 CCK (195 +/- 14 ml; not significant). During both isovolumetric and isobaric distensions, 1.0 IDU.kg-1.h-1 CCK significantly (P < 0.05) increased proximal gastric compliance compared with saline. However, 0.5 IDU.kg-1.h-1 CCK had no significant effect on gastric compliance. During volume distensions, but not during fixed pressure distensions, 1.0 IDU.kg-1.h-1 CCK significantly (P < 0.05) reduced visceral perception. These results suggest that in humans CCK may have a physiological role in regulating proximal gastric mechanics.

Adult↗

PubMed1998

Effect of medium- and long-chain triglycerides on lower esophageal sphincter pressure: role of CCK.

Fat meals are known to decrease lower esophageal sphincter (LES) pressure, possibly through postprandial CCK release. Dietary fat consists mainly of long-chain triglycerides (LCT), which potently stimulate CCK secretion. This effect contrasts with that of medium-chain triglycerides (MCT), which do not induce CCK release. We recorded LES pressure and gallbladder volume in six healthy subjects on five separate occasions during intraduodenal administration of 1) saline control, 2) LCT, 3) MCT, 4) LCT during intravenous infusion of the CCK receptor antagonist loxiglumide, and 5) MCT together with loxiglumide. LES pressure decreased significantly during administration of both LCT and MCT. Loxiglumide completely prevented the reduction in LES pressure during intraduodenal LCT, but not during intraduodenal MCT. Gallbladder volume decreased during LCT, but not during MCT. It is concluded that intraduodenal administration of equimolar amounts of both LCT and MCT significantly reduces LES pressure. The effect of LCT on LES pressure is mediated by CCK. The effect of MCT is not dependent on CCK, since MCT does not release CCK and loxiglumide does not prevent the MCT-induced reduction in LES pressure.

Adult↗