The Effect of Unenhanced MRI on the Surgeons' Decision-Making Process in Females with Suspected Appendicitis.

BACKGROUND: This prospective study evaluated the impact of the results of unenhanced magnetic resonance imaging (MRI) on the surgeon's diagnosis of acute appendicitis in potentially fertile females. METHODS: 112 female patients, aged 12-55, with suspected appendicitis underwent MRI of the abdomen. At three defined intervals; admission and clinical re-evaluation before and after revealing the MRI results, the surgeon recorded the attendance of each patient in operative treatment, observation or discharge. Appendicitis was confirmed or declined by pathology or by telephone follow-up in case of non-intervention. FINDINGS: Appendicitis was confirmed in 29 of 112 patients. At admission the surgeon's disposition had a sensitivity of 97 % and specificity of 29 %. After knowing the MRI results, sensitivity was 97 % and specificity 64 %. The sensitivity and specificity of MRI alone were 89 and 100 %, with a negative and positive predictive value of 96 and 100 %, respectively. CONCLUSION: We believe that MRI should perhaps be standard in all female patients during their reproductive years with suspected appendicitis. It avoids an operation in 32 % of cases and allows earlier planning for patients with an equivocal clinical picture. Trial number: OND1292733 (Narcis.nl).

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.

Post-prandial intragastric and duodenal acidity are increased in patients with chronic pancreatitis.

OBJECTIVES: Patients with chronic pancreatitis and exocrine insufficiency have lower intraduodenal pH compared to controls. It has been assumed that abnormal low intraduodenal pH in these patients not only results from impaired pancreatic bicarbonate secretion but also from an increased gastric acid load to the duodenum. METHODS: We have tested this hypothesis by combined intragastric and intraduodenal 24 h pH monitoring in nine chronic pancreatitis patients with exocrine pancreatic insufficiency and nine healthy control subjects during standardized test conditions. Postprandial gastrin and cholecystokinin release were also determined. RESULTS: Median 24-h intraduodenal pH (5.90 vs. 6.00) and intragastric pH (1.60 vs. 1.70) were not significantly different between patients and controls. However, in the 2-h postprandial periods intraduodenal pH was below five for a significantly higher percentage of time in chronic pancreatitis patients compared to controls (lunch: 14.5% vs. 0.17%, P=0.011; dinner: 24.1% vs. 5.75%, P=0.05). The post-dinner intragastric pH was below three for a significantly higher percentage of time in chronic pancreatitis patients vs. controls (72.2 vs. 48.9%, P=0.04). Postprandial gastrin release was not significantly different between the two groups. Postprandial secretion of cholecystokinin (CCK), as enterogastrone, was significantly (P < 0.01) reduced in chronic pancreatitis patients (78 +/- 13 pmol/L, 120 min) compared to controls (155 +/- 14 pmol/L, 120 min). CONCLUSIONS: Median intraduodenal and intragastric pH are not significantly decreased in patients with chronic pancreatitis and exocrine insufficiency but the postprandial time with an acidic pH in the duodenum (pH < 5) and in the stomach (pH < 3) is significantly (P

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.

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.

Reproducibility of antroduodenal motility during prolonged ambulatory recording.

Ambulatory recording of antroduodenal manometry is a novel technique with several advantages over standard stationary manometry recording. Although the feasibility of this technique in clinical practice has been demonstrated, reproducibility of antroduodenal motility recorded by means of ambulatory manometry has not been investigated. To test whether antroduodenal motility recorded by ambulatory manometry is reproducible, we performed two 24-h ambulatory antroduodenal manometry recordings in 18 healthy subjects according to an identical protocol with a 1-week interval. Motility was recorded with a five-channel solid-state catheter. Postprandial motility was recorded after consumption of two test meals and interdigestive motility was recorded nocturnally. Postprandial antroduodenal motor characteristics were identical between the separate recordings. The number and duration of nocturnal cycles of the interdigestive migrating motor complex were also in the same range. Phase III characteristics in general were not different between the two recordings. Only minor alterations were observed in the duration of phase III motor fronts with duodenal onset and in the number of interdigestive cycles concluded by duodenal onset phase III. Parameters obtained by qualitative analysis were comparable between the two recordings. The antroduodenal motility pattern, when measured by ambulatory recording with solid state catheters under standardized conditions, is very reproducible.

Cholecystokinin secretion in patients with chronic pancreatitis and after different types of pancreatic surgery.

UNLABELLED: Cholecystokinin (CCK) secretion may be affected in patients with chronic pancreatitis (CP), but little is known on the effect of pancreatic surgery on CCK secretion. We measured CCK secretion (radioimmunoassay, RIA) in response to bombesin infusion (100 ng/kg/20 min) for 120 min to test CCK secretory capacity, to ingestion of a liquid diet (400 kcal) for 120 min, and in response to a solid fat-rich meal (500 kcal) for 120 min. These studies were performed in 45 patients with CP (25 with exocrine insufficiency), 15 patients after duodenum-preserving pancreatic head resection (DPRHP), 18 patients after the Whipple operation, 12 patients after distal pancreatectomy (DP), and 35 control subjects. In CP patients, the CCK secretory capacity was preserved, but the postprandial CCK response was reduced, depending on meal composition and the presence of exocrine insufficiency. In patients after Whipple's operation, CCK secretory capacity and postprandial CCK secretion were significantly (p < 0.05) reduced. In patients after DPRHP, CCK secretory capacity was not affected, but the postprandial CCK response was significantly (p < 0.05) reduced, depending on meal composition and the presence of exocrine insufficiency. In patients after DPRHP, fasting plasma CCK levels were significantly (p < 0.01) increased, pointing to the absence of feedback inhibition on CCK secretion by intraluminal enzymes. After DP, the CCK secretory capacity was not affected. IN CONCLUSION: alterations in CCK secretion are observed in patients with chronic pancreatitis and after pancreatic surgery. These alterations are related not only to the disease process (exocrine insufficiency) but also to the type of surgery and type of stimulus.

Effect of insulin and glucose on basal and cholecystokinin-stimulated exocrine pancreatic secretion in humans.

Pancreaticobiliary secretion is reduced during acute hyperglycemia. In nondiabetics, this inhibitory effect also may result from hyperinsulinemia. Therefore we investigated the effects of acute hyperglycemia and euglycemic hyperinsulinemia on basal and cholecystokinin (CCK)-stimulated pancreaticobiliary secretion. Nine healthy volunteers (age, 22-52 years) were studied on three occasions in random order during (a) intravenous saline (control), (b) hyperglycemic hyperinsulinemic clamping (HG; plasma glucose at 15 mM), and (c) euglycemic hyperinsulinemic clamping (HI; plasma insulin at 150 mU/L, glucose at 4-5 mM). Duodenal outputs of bilirubin, amylase, trypsin, and bicarbonate were measured under basal conditions and during CCK infusion (0.25 and 0.5 IDU/kg/h). Basal pancreaticobiliary secretion was significantly (p < 0.05) reduced during both HG and HI. During low-dose CCK stimulation, HG significantly (p < 0.05) reduced bilirubin and trypsin output compared with control. In contrast, HI did not significantly reduce pancreatic enzyme and bilirubin output during low-dose CCK infusion. During high-dose CCK infusion, neither HI nor HG influenced pancreatic enzyme and bilirubin output. Pancreatic bicarbonate output was not influenced by CCK and remained significantly (p < 0.05) reduced during HI and HG compared with control. It is concluded that during both acute hyperglycemia and euglycemic hyperinsulinemia, basal pancreaticobiliary secretion is significantly reduced. CCK-stimulated pancreatic enzyme and bilirubin output is significantly reduced only during hyperglycemia. The inhibitory effect of hyperglycemia on pancreaticobiliary secretion in healthy volunteers may occur independent of insulin.

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.

The role of cholecystokinin and the cholinergic system in intravenous amino acid-induced gallbladder emptying.

BACKGROUND: Recent studies have demonstrated that separate intravenous infusion of amino acids (IVAA) at high doses induces gallbladder emptying. However, little is known about the mechanisms mediating IVAA-induced gallbladder contraction. OBJECTIVE AND METHODS: To investigate whether the effect of IVAA on gallbladder motility is mediated by the cholinergic system and/or cholecystokinin (CCK), the major hormonal stimulus for gallbladder contraction. Six healthy male volunteers were studied in random order on five occasions using: (a) IVAA, (b) loxiglumide (CR 1505, a selective CCK-A receptor antagonist), (c) IVAA plus loxiglumide, (d) atropine and (e) IVAA plus atropine. Gallbladder volumes (ultrasonography) and plasma CCK levels (radioimmunoassay) were determined every 15 min for 60 min before and for 120 min during intravenous infusion of amino acids (Vamin 18EF; 250 mg protein/kg/h) and/or loxiglumide (10 mg/kg/h) and/or atropine (0.005 mg/kg/h). RESULTS: IVAA significantly (P < 0.05) reduced gallbladder volume from 32 +/- 5 ml to 17 +/- 2 ml but induced only a small and transient increase in plasma CCK levels. Loxiglumide given alone significantly (P < 0.05) increased fasting gallbladder volume to 190% of the basal value. IVAA-induced gallbladder emptying was completely abolished by loxiglumide. Maximal gallbladder relaxation during IVAA plus loxiglumide was not significantly different compared to loxiglumide given alone. Concomitant administration of atropine also significantly (P < 0.05) inhibited IVAA-induced gallbladder emptying. CONCLUSION: In healthy volunteers intravenous infusion of high doses of amino acids results in a significant gallbladder contraction, which is inhibited by CCK-A receptor blockade and by atropine.

Effect of i.v. amino acids on satiety in humans.

BACKGROUND: Parenteral nutrients suppress oral food intake. Separate i.v. infusion of amino acids (IVAA) at high doses affects gastrointestinal motility and secretion. However, little is known on the effects of separate i.v. infusion of amino acids at these high doses on satiety. Therefore, we have studied the effect of two different doses of a commercially available mixed amino acids solution on satiety and food intake. METHODS: Six healthy volunteers (ages 20 to 34 years) were studied on three separate occasions in random order during (a) i.v. saline (control), (b) low-dose IVAA ([LDA] 125 mg protein/kg/h, Vamin 18EF; Kabi Pharmacia BV, Woerden, The Netherlands), or (c) high-dose IVAA ([HDA] 250 mg protein/kg/h) for 360 minutes. Subjective criteria such as wish to eat, prospective feeding intentions, and feelings of hunger and fullness were scored on 100-mm visual analog scales at 30-minute intervals. Food preference also was measured every 60 minutes with food selection lists. At the end of the experiment a meal was presented. RESULTS: Feelings of fullness were significantly (p < .05) increased during both LDA and HDA. The wish to eat was significantly (p < .05) decreased during HDA compared with control and LDA. Prospective feeding intentions also tended to be reduced during HDA (not significant). Feelings of hunger were not significantly different between the three experiments. Total food selection was significantly (p < .05) decreased during LDA and HDA, mainly because of a significantly (p < .05) decreased preference for fat-rich items. However, the total amount of food consumed at the end of the experiment was not significantly different between the three experiments. CONCLUSIONS: The present study shows that in healthy volunteers, IVAA (1) increase satiety ratings, (2) increase feelings of fullness, (3) decrease preprandial food selection, and (4) have no effect on subsequent oral food intake.

Effects of parenteral nutrients on gastrointestinal motility and secretion.

BACKGROUND: The stimulation of gastrointestinal motility and secretion during nutrient digestion is generally divided into a cephalic, gastric and intestinal phase. Little is known about the effects of macronutrients on gastrointestinal function during the postabsorptive or circulatory phase of digestion. METHODS: Review of studies investigating the effects of circulating macro-nutrients such as fat, amino acids and glucose on gastrointestinal motility and secretion. RESULTS: Intravenous infusion of fat emulsions delays gastric emptying and interrupts the interdigestive intestinal motor pattern. Intravenous amino acids, administered in high doses, stimulate gastric acid secretion, pancreatic secretion, gallbladder contraction, and intestinal motility. Patients receiving total parental nutrition (TPN) have inert gallbladders and are at risk of developing gallbladder sludge and stones. Administering a proportion of the daily amino acid requirement by rapid intravenous infusion may prove useful in the prevention of sludge and stone formation during TPN by promoting gallbladder contraction. Intravenous infusion of glucose, already at physiological postprandial plasma levels, inhibits gastrointestinal motility and secretion. The inhibitory effect of glucose is dose-dependent, that is, more pronounced at higher plasma glucose levels. Recent studies have indicated that in patients with diabetes mellitus alterations in gastrointestinal function are related to the degree of hyperglycaemia. CONCLUSIONS: Nutrients during the circulatory phase of digestion influence gastrointestinal motility and secretion. Knowledge of these effects is relevant for conditions with increased plasma levels of macro-nutrients such as in patients with diabetes mellitus or during total parenteral nutrition.

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.

Vasoactive substances in early dumping syndrome: effects of dumping provocation with and without octreotide.

In patients after gastric surgery, early dumping symptoms can be provoked by oral glucose challenge. Octreotide effectively prevents the occurrence of dumping symptoms. We have studied plasma renin activity (PRA), aldosterone and atrial natriuretic peptide (ANP) concentrations in nine patients with early dumping, 10 surgical control subjects and nine healthy control subjects after an oral glucose challenge preceded by either placebo or 25 micrograms of octreotide subcutaneously (s.c.). In the dumping group, basal PRA was significantly (P < 0.01) higher (3.9 +/- 0.6 micrograms L-1 h-1) than in either surgical or healthy control subjects (1.1 +/- 0.3 micrograms L-1 h-1 and 1.1 +/- 0.2 micrograms L-1 h-1 respectively) and showed a significant rise after glucose ingestion to 5.4 +/- 0.9 micrograms L-1 h-1 that did not occur in control subjects. Aldosterone concentration showed a concomitant rise. In dumping patients, plasma ANP decreased after glucose ingestion from 31 +/- 6 ngL-1 to 21 +/- 5 ngL-1 (P < 0.05). This decrease did not occur in control subjects. Early dumping is associated with an activation of the renin-aldosterone axis and a decrease in plasma ANP, reflecting a hypovolaemic state. Octreotide prevents the occurrence of these changes.

Is the effect of acute hyperglycaemia on interdigestive antroduodenal motility and small-bowel transit mediated by insulin?

Acute hyperglycaemia inhibits antroduodenal motility. In non-diabetic subjects this inhibitory effect may result from reactive endogenous hyperinsulinaemia. Therefore, we investigated the effects of hyperinsulinaemia during both hyperglycaemia and euglycaemia on interdigestive antroduodenal motility (perfusion manometry) and duodenocaecal transit time (DCTT; lactulose breath-H2 test). Six healthy volunteers (age 20-26 years) were studied for 240 min on three separate occasions in random order during: (a) i.v. saline (control); (b) acute hyperglycaemic hyperinsulinaemia (HG) with plasma glucose at 15 mmolL-1; and (c) euglycaemic hyperinsulinaemia (HI) with plasma insulin at 80 mUL-1 and glucose at 4-5 mmolL-1, RESULTS: DCTT was significantly (P < 0.05) prolonged during HG (158 +/- 23 min) compared with control (95 +/- 25 min), whereas HI had no effect (100 +/- 17 min). Mean duration of complete migrating motor complex (MMC) cycles was significantly (P < 0.05) reduced during HG (63 +/- 9 min) compared with control (103 +/- 15 min) and HI (105 +/- 16 min), which resulted from a significantly (P < 0.05) shorter duration of phase II. Antral motility was significantly (P < 0.05) reduced during both HI (20 +/- 8 contractions 240 min-1) and HG (9 +/- 5) compared with control (43 +/- 7). It is concluded that in healthy subjects hyperglycaemia prolongs DCTT, increases duodenal MMC cycle frequency and inhibits antral motility. Hyperinsulinaemia reduces antral motor activity but has no effect on interdigestive duodenal motility or DCTT. Thus, other factors, apart from insulin, mediate the inhibitory effect of hyperglycaemia on interdigestive intestinal motility and transit.

Effects of medium-chain and long-chain triglycerides on antroduodenal motility and small bowel transit time in man.

UNLABELLED: Medium-chain triglycerides are known to induce diarrhea, possibly resulting from accelerated intestinal transit. We performed antroduodenal manometry and lactulose hydrogen breath testing simultaneously in eight healthy subjects in order to determine the effects of intraduodenally administered medium-chain triglycerides (MCT) and long-chain triglycerides (LCT) on gastrointestinal motility and small bowel transit time. LCT (15 mmol/hr) induced a fed motor pattern. In contrast, during MCT, in both equimolar (15 mmol/hr; MCT-1) and equicaloric (30 mmol/hr; MCT-2) amounts comparable to LCT, interdigestive motility was preserved but with a significantly (P < 0.05) shorter MMC cycle length (MCT-1, 65 +/- 7 min; MCT-2, 53 +/- 6 min) compared to control (saline infusion; 127 +/- 14 min). Duodenocecal transit time (DCTT) was significantly (P < 0.05) accelerated during administration of MCT (MCT-1, 56 +/- 6 min; MCT-2, 69 +/- 9 min) and was not affected by LCT (105 +/- 13 min) when compared to control (101 +/- 9 min). IN CONCLUSION: MCT, in contrast to LCT, preserve interdigestive motility with a shorter MMC cycle length and accelerate DCTT.

Effect of gastrin on antroduodenal motility: role of intraluminal acidity.

The effect of gastrin on the migrating motility complex (MMC) was studied in seven healthy subjects. It was hypothesized that a potential effect of gastrin on the MMC may result from intraluminal acidification through increased gastric acid secretion. Therefore, antroduodenal manometry and intraluminal acidity were recorded simultaneously. The effect of gastric acid inhibition, with and without administration of gastrin, on antroduodenal motility and intraluminal acidity was also evaluated and compared with saline infusion (control). Continuous infusion of gastrin-17 (20 pmol. kg-1. h-1) increased intragastric and intraduodenal acidity and suppressed phase II and phase III motor activity in both antrum and duodenum. Concomitant gastric acid inhibition with intravenous famotidine, as demonstrated by intragastric neutralization of pH, completely antagonized the effect of gastrin on the MMC. In fact, famotidine infusion, both with and without administration of gastrin, significantly shortened MMC cycle length. It is concluded that the effect of gastrin on interdigestive antroduodenal motility results from increased intraluminal acidity.

Gall bladder emptying in severe idiopathic constipation.

BACKGROUND: It has been suggested that slow transit constipation (STC) may be part of a panenteric motor disorder. AIM: To evaluate motility of an upper gastrointestinal organ, the gall bladder, in 16 patients with STC and 20 healthy controls. METHODS: Gall bladder emptying (ultrasonography) was studied in response to neural, cephalic-vagal stimulation with modified sham feeding (MSF) for 90 minutes and in response to hormonal stimulation with cholecystokinin (CCK, 0.5 IDU/kg/h) for 60 minutes. RESULTS: Fasting gall bladder volume in patients with STC (17 (2) cm(3)) was significantly (p<0. 01) reduced compared with that in controls (24 (2) cm(3)). Gall bladder emptying in response to MSF was significantly reduced in patients with STC expressed both as percentage emptying (11 (5)% versus 22 (3)%; p<0.05) and as absolute emptying (2.1 (0.7) cm(3) versus 4.9 (0.7) cm(3); p<0.02). However, percentage gall bladder emptying in response to CCK was not different between patients and controls (73 (4)% versus 67 (4)%) although the absolute reduction in gall bladder volume was significantly (p<0.05) smaller in patients (10.7 (1.1) cm(3) versus 15.3 (1.4) cm(3)). CONCLUSIONS: Patients with slow transit constipation have smaller fasting gall bladder volumes, impaired gall bladder responses to vagal cholinergic stimulation, but normal gall bladder responses to hormonal stimulation with CCK. These results point to abnormalities in gastrointestinal motility proximal from the colon in slow transit constipation and more specifically, impaired neural responsiveness.

Gallbladder motility in response to sham feeding and cholecystokinin in lean and obese subjects.

The risk of developing gallstones is increased in obese subjects. We have investigated whether gallbladder motility in obese subjects is different from that in lean control subjects. In 25 healthy non-diabetic obese subjects and 20 age- and sex-matched lean controls, fasting gallbladder volumes, gallbladder contraction in response to cephalic vagal cholinergic stimulation by modified sham feeding (MSF) and to hormonal stimulation with cholecystokinin (CCK) were studied. Gallbladder volumes were measured during a 30-min MSF period followed 1 h later by a 1-hour continuous i.v. infusion of 0.5 IDU/kg ideal weight of CCK-33. Fasting gallbladder volumes were significantly (p < 0.001) larger in obese (47 +/- 4 cm3) compared to lean subjects (24 +/- 2 cm3). Fasting gallbladder volume was correlated with body mass index (p < 0.01). Gallbladder contraction during MSF was significantly (p < 0.01) reduced in obese (12 +/- 2%) compared to lean subjects (22 +/- 3%). CCK infusion, leading to physiological post-prandial plasma CCK levels, induced a significantly (p < 0.001) greater absolute gallbladder contraction in obese (27 +/- 3 cm3) compared to lean subjects (15 +/- 1 cm3) but the percentage gallbladder contraction was in the same range (64 +/- 3% vs. 67 +/- 4%, respectively). In addition, residual gallbladder volumes after CCK infusion were significantly (p < 0.001) larger in obese (15 +/- 2 cm3) than in lean subjects (7 +/- 1 cm3). Two groups of obese subjects were identified: one with increased (>40 cm3) and one with normal (< or = 40 cm3) fasting gallbladder volumes. Only obese subjects with increased fasting volumes showed abnormal gallbladder motility.