Biomedical subjects

C Feinle

Publications and source records attributed to C Feinle.

11 recordsLinked to original sources

PubMed1999

Assessment of gastric motor function during the emptying of solid and liquid meals in humans by MRI.

Gastric emptying and motility have previously been assessed by magnetic resonance imaging (MRI) using liquid test meals. The aim of this study was to extend the applicability of our MRI method to the assessment of gastric emptying and motility of solid meals. Gastric emptying and motility of a liquid and a solid meal, of similar chemical properties, were studied in eight volunteers. The MRI protocol combined a multislice turbo spin-echo (TSE) sequence (volume scan, resolution: 1.5 mm) and a dynamic FFE sequence (motility scan, 1 sec/image, resolution: 3.1 mm). Gastric emptying of the liquid meal was faster than emptying of the solid meal when considering half-times of emptying. However, during the first 15 minutes after ingestion, the liquid meal emptied more slowly. This was related to reduced motility with the liquid meal. In conclusion, with our MRI method it is feasible to assess gastric emptying and motility of liquid and solid meals.

Adult↗

PubMed1999

Scintigraphic validation of a magnetic resonance imaging method to study gastric emptying of a solid meal in humans.

BACKGROUND: We have previously used a magnetic resonance imaging (MRI) method to study gastric emptying of liquids. So far, however, it has not possible to assess solid gastric emptying with this technique. AIMS: To validate scintigraphically MRI as a method for measuring emptying of a mixed solid/liquid meal. METHODS: In eight healthy subjects, gastric emptying of a solid/liquid (SM) and a liquid meal (LM) of identical energy content and macronutrient composition was studied by scintigraphy and MRI for 120 minutes. RESULTS: MRI and scintigraphy agreed with respect to emptying profiles (intraclass correlation coefficient (RI) SM: 0.988, RI, LM: 0.917), t1/2 (SMMRI: 129 (9), SMScinti: 123 (11) minutes, NS; LMMRI: 100 (7), LMScinti: 110 (8) minutes, NS) and AUC (SMMRI: 8999 (232), SMScinti: 8788 (277) min%, NS; LMMRI: 8819 (368), LMScinti: 8891 (321) min%, NS). CONCLUSIONS: MRI can be used to measure reliably gastric emptying not only of liquid but also of mixed solid/liquid meals in humans.

Adult↗

PubMed1998

Duodenal sensitivity to lipids and gastric motility: contribution to functional dyspepsia.

The term "functional dyspepsia" represents a complex of symptoms related to the upper gastrointestinal tract, including epigastric pain, upper abdominal bloating/distension, regurgitation, postprandial fullness, early satiety, nausea and vomiting and frequently reported to occur in connection with food intake. Particularly foods containing fat appear to potently provoke dyspeptic symptoms. Despite all the anecdotal reports from patients as to which food groups or even particular nutrients evoke symptoms, it is rather surprising that only few studies have been published which systematically investigate the effects of these foods or the exclusion of certain foods on symptom development and improvement. The results from these studies were not clear-cut: although some patients report to experience dyspeptic symptoms after foods rich in fat, they tolerate these foods if the fat is well disguised [1]. In addition, food consistency or preparation appears to be a determinant for symptoms: solid food containing fat is less likely to induce symptoms than fat-containing liquids [2]. The following discussion will be focussed on the role of gastric motility and gastrointestinal sensitivity to nutrients and a possible interaction between the two in the origin of symptoms of functional dyspepsia.

Chemoreceptor Cells↗

PubMed1998

Role of intestinal chemoreception in the induction of gastrointestinal sensations.

Both distension of the stomach and activation of small intestinal chemoreceptors by nutrients have been implicated in the induction of postprandial sensations. Studies were performed in healthy human subjects to investigate the roles of gastric distension and activation or inhibition of small intestinal chemoreceptors in the generation of pleasant (fullness) and unpleasant (nausea, pain) gastrointestinal sensations. The proximal stomach was distended by inflating a balloon attached to a gastric tube with air, while the duodenum was perfused with nutrient solutions, either lipid or carbohydrates. In additional experiments, the upper small intestinal mucosa was anaesthetised by topical anaesthesia or an antagonist to cholecystokinin (CCK)-A receptors given intravenously during duodenal lipid infusion. Gastric distension induced sensations of epigastric pressure and pain, while during duodenal infusion of both carbohydrate and lipid, fullness was described as a more meal-like sensation. In addition, lipid but not carbohydrate infusion resulted in significant nausea. The sensory experience evoked by lipid was diminished by both topical mucosal anaesthesia and CCK-A receptor blockade. The data provide evidence for the involvement of small intestinal chemoreceptors in the modulation of sensations induced by gastric distension.

Adult↗

PubMed1997

Effects of duodenal nutrients on sensory and motor responses of the human stomach to distension.

To study in healthy subjects the relationship between gastric sensations/perception and motility during gastric distension and the effects of duodenal nutrients, a flaccid gastric bag was distended in the proximal stomach with air at 100 ml/min while the duodenum was perfused (1 ml/min) with isotonic saline, hypertonic saline, glucose (1 kcal/ml), maltodextrin (2 kcal/ml), and 10% (1 kcal/ml) and 20% lipid (2 kcal/ml). Intragastric pressure was recorded continuously, and the subjects were asked to report gastric sensations. Compared with isotonic saline, all infusions significantly decreased gastric tonic and phasic pressure activity during gastric distensions and, with the exception of 20% lipid, caused fullness and discomfort during distensions to occur at larger volumes associated with lower intragastric pressures. Maltodextrin and 20% lipid changed fullness during distensions into a meal-like sensation. Only 20% lipid significantly increased the incidence of nausea. In conclusion, the sensory responses to gastric distension are modified by duodenal nutrients. Different nutrients result in different responses, but the responses obtained cannot be explained by changes in gastric pressure activity.

Adult↗

PubMed1997

[Functional dyspepsia].

The term "functional dyspepsia" describes a complex of symptoms which are related to the upper gastrointestinal tract and frequently experienced by the patients after food intake. The pathophysiology of functional dyspepsia is still poorly understood. There are no organic causes found nor are there any functional changes observed that correlate with symptom occurrence and intensity and which could offer a satisfactory explanation for the symptoms and a basis for successful therapy. Mechanisms discussed include a disturbance of gastric motility and emptying, an increased sensitivity of the stomach to or hypersecretion of gastric acid, and infection by Helicobacter pylori. Recent research indicates visceral hypersensitivity of the gastroduodenal region to mechanical (distension) and chemical (nutrients or neuromodulators) stimulation to be a major factor in the aetiology of functional dyspepsia, potentially offering an explanation why dyspeptic symptoms are often related to food intake. The occurrence of dyspeptic symptoms in relation to food ingestion frequently prompts the gastroenterologist to the diagnosis of a motility disorder and subsequent therapy with prokinetic drugs. These substances may result in an improvement of gastric emptying, but not necessarily symptoms. It is apparent that the incompletely understood pathophysiology of functional dyspepsia is one of the main reasons for the lack of an effective therapy for this common condition.

Diagnosis, Differential↗

PubMed1996

Cholecystokinin-A receptors modulate gastric sensory and motor responses to gastric distension and duodenal lipid.

BACKGROUND & AIMS: The combination of duodenal lipid and gastric distention induces meal-like fullness followed by nausea in healthy subjects. The aim of this study was to assess the role of cholecystokinin (CCK) A receptors in these changes using a CCK-A antagonist loxiglumide. METHODS: Twelve healthy subjects were studied on four occasions, during which either 0.9% saline or 20% Intralipid was infused intraduodenally on two occasions each (1 mL/min) while the proximal stomach was distended with air (100 mL/min). During each duodenal infusion, subjects received intravenous loxiglumide (10 mg.kg-1.h-1) on 1 day and placebo on the other. Intragastric pressure changes were recorded, and the subjects reported gastric sensations (fullness, nausea). RESULTS: Loxiglumide did not influence gastric motility or sensitivity during duodenal saline infusion. Duodenal lipid reduced gastric tonic and phasic pressure activity during distensions and induced meal-like fullness and nausea; sensations were reported at similar volumes but lower intragastric pressures (P < 0.001 vs. saline). Loxiglumide partially restored gastric tonic and phasic activity during lipid infusion, reduced the occurrence of meal-like fullness and nausea, and increased the pressures at which sensations were reported (P < 0.001 vs. placebo). CONCLUSIONS: CCK-A receptors are involved in the induction of meal-like fullness and nausea associated with intraduodenal lipid and gastric distention.

Adult↗

PubMed1996

Ondansetron reduces nausea induced by gastroduodenal stimulation without changing gastric motility.

The involvement of 5-hydroxytryptamine3 (5-HT3) receptors in gastric motor and sensory responses to distension and duodenal lipid was investigated. Subjects were studied on four occasions during which isotonic saline or 20% Intralipid (2 kcal/ml) was infused intraduodenally (1 ml/min) while the proximal stomach was distended with air (100 ml/min). Subjects received either 8 mg ondansetron (5-HT3 antagonist) or placebo orally in random order. Intragastric pressure was recorded continuously, and subjects reported gastric sensations. Gastric motor and sensory responses to distension during duodenal saline were similar with placebo and ondansetron. Intraduodenal lipid decreased gastric tonic and phasic pressure activity, and this was not influenced by ondansetron. Lipid also induced meal-like fullness followed by nausea during distensions. Ondansetron reduced nausea and did not affect meal-like fullness but increased volumes and pressures at which sensations were reported. Intestinal 5-HT3 receptors are involved in induction of nausea but not of meal-like fullness by intraduodenal lipid and gastric distension. 5-HT3 receptor antagonism reduces gastric sensitivity to distension during intraduodenal lipid infusion.

Adult↗

PubMed1995

Nutrient-specific modulation of gastric mechanosensitivity in patients with functional dyspepsia.

Intraduodenal lipid infusion induces symptoms and increases sensitivity to gastric distension in patients with functional dyspepsia. To test whether these effects are specific for lipid, we compared the effects of intraduodenal infusions of either lipid or glucose on symptoms and gastric sensory and motor responses to gastric distension. Eighteen dyspeptic patients and nine controls were studied. The stomach was distended with a flaccid bag during isocaloric infusions (1 kcal/ml) of saline and either 10% Intralipid (nine patients) or 26.7% glucose (nine patients) into the duodenum. Dyspeptic symptoms and sensory thresholds for epigastric fullness and discomfort were assessed. Gastric pressure profiles during distensions were similar during lipid and glucose infusions in patients and controls, but both were significantly lower than during saline infusion. Lower volumes were required to induce fullness and discomfort in the patients compared with the controls. In the controls, the threshold volumes required to induce fullness and discomfort were greater during infusion of lipid and glucose than during saline infusion, but in the patients, the threshold volumes were increased during glucose infusion but further reduced during lipid infusion. Moreover, in the patients, nausea was more common during lipid than glucose infusion and did not occur during saline. The controls did not experience any symptoms during any infusion. In conclusion, intraduodenal lipid but not glucose sensitizes the stomach to distension in patients with functional dyspepsia but not in controls.

Adult↗

PubMed1995

Fat increases vection-induced nausea independent of changes in gastric emptying.

Vection and fat delay gastric emptying and can induce nausea. Therefore, we studied the interaction between vection and fat on the production of nausea and the relationship between the severity of symptoms and changes in gastric emptying. Twelve healthy males consumed two liquid test meals, a zero-fat and a high-fat meal. Nausea was induced by seating the subjects inside a rotating vection drum. In protocol 1, drum rotation started immediately after ingestion of either meal; in protocol 2, when approximately 50% of each meal had emptied into the intestine. Gastric emptying was determined using gamma scintigraphy. Severity of symptoms was assessed throughout. Symptoms were similar for the high-fat and the zero-fat meal when vection was induced immediately after meal ingestion. Scores were only elevated by the high-fat meal when about half the meal had entered the intestine before vection was induced. No correlation was found between gastric emptying and the severity of symptoms. In conclusion, the interaction of vection and intraduodenal fat exacerbates nausea, but this effect is independent of a delay in gastric emptying.

Adult↗

PubMed1995

Abnormal sensitivity to duodenal lipid infusion in patients with functional dyspepsia.

BACKGROUND AND OBJECTIVES: Patients with functional dyspepsia exhibit increased sensitivity to gastric distension (mechanoreceptors) and to meals rich in fat (chemoreceptors). The aim of this study was to test whether these patients were abnormally sensitive to intraduodenal lipid, and whether this stimulus altered gastric mechanosensitivity. METHODS AND DESIGN: Experiments were conducted on 10 patients and 10 healthy controls. The stomach was distended with a flaccid bag during duodenal infusion of either 10% Intralipid or 0.9% saline. Intragastric pressure was recorded continuously, and the participants were asked to report gastric sensations of fullness and discomfort. RESULTS: Intragastric pressure profiles during distension were similar in patients and controls. Lipid decreased intragastric pressure and reduced phasic contractility. Patients showed enhanced sensitivity to gastric distension compared with controls during both saline and lipid infusions. In the controls, threshold volumes for fullness and discomfort were higher during lipid than saline infusion. In the patients, the sensation of fullness occurred at lower volumes during lipid infusion, whereas discomfort occurred at similar volumes but lower intragastric pressures. Most patients experienced nausea and bloating and three patients vomited during lipid infusion, but remained asymptomatic during saline infusion. Controls reported no symptoms during either infusion. CONCLUSION: Dyspeptic patients have increased sensitivity to both gastric distension and intraduodenal lipid. In contrast to controls, lipid sensitizes their stomachs to distension.

Abdominal Pain↗