scholarly journals Motor function of the proximal stomach and visceral perception in gastro-oesophageal reflux disease

Gut ◽  
1998 ◽  
Vol 42 (2) ◽  
pp. 251-257 ◽  
Author(s):  
R Penagini ◽  
G Hebbard ◽  
M Horowitz ◽  
J Dent ◽  
H Bermingham ◽  
...  
Keyword(s):  
Motor Function ◽  
Reflux Disease ◽  
Lower Oesophageal Sphincter ◽  
Visceral Sensitivity ◽  
Visceral Perception ◽  
Proximal Stomach ◽  
Gastric Tone ◽  
Gastric Motor Function ◽  
Delayed Recovery ◽  
Historical Controls

Background—The abnormally high postprandial rate of transient lower oesophageal sphincter relaxations seen in patients with reflux disease may be related to altered proximal gastric motor function. Heightened visceral sensitivity may also contribute to reporting of symptoms in these patients.Aims—To assess motor function of the proximal stomach and visceral perception in reflux disease with a barostat.Methods—Fasting and postprandial proximal gastric motility, sensation, and symptoms were measured in nine patients with reflux disease and nine healthy subjects. Gastric emptying of solids and liquids was assessed in six of the patients on a different day (and compared to historical controls).Results—Minimal distending pressure and gastric compliance were similar in the two groups, whereas the patients experienced fullness at lower pressures (p<0.05) and discomfort at lower balloon volumes (p<0.005) during isobaric and isovolumetric distensions respectively. Maximal gastric relaxation induced by the meal was similar in the two groups. Late after the meal, however, proximal gastric tone was lower (p<0.01) and the score for fullness higher (p<0.01) in the reflux patients, in whom the retention of both solids and liquids in the proximal stomach was greater (p<0.05).Conclusions—Reflux disease is associated with delayed recovery of proximal gastric tone after a meal and increased visceral sensitivity. The former may contribute to the increased prevalence of reflux during transient lower oesophageal sphincter relaxations and the delay in emptying from the proximal stomach, whereas both may contribute to symptom reporting.

Proximal gastric motor function in reflux disease and after laparoscopic fundoplication

1998 ◽  
Vol 114 ◽  
pp. A856
Author(s):  
M.K. Vu ◽  
P.J. van der Schaar ◽  
J.W.A. Straathof ◽  
C.B.H.W. Lamers ◽  
A.A.M. Masclee
Keyword(s):  
Motor Function ◽  
Reflux Disease ◽  
Laparoscopic Fundoplication ◽  
Gastric Motor Function

scholarly journals Effects of somatostatin on proximal gastric motor function and visceral perception

1998 ◽  
Vol 12 (11) ◽  
pp. 1163-1169 ◽  
Author(s):  
Mearadji ◽  
Straathof ◽  
Biemond ◽  
Lamers ◽  
Masclee
Keyword(s):  
Motor Function ◽  
Visceral Perception ◽  
Gastric Motor Function

Glucose acts in the CNS to regulate gastric motility during hypoglycemia

2003 ◽  
Vol 285 (5) ◽  
pp. R1192-R1202 ◽  
Author(s):  
Min Shi ◽  
Allison R. Jones ◽  
Mark S. Niedringhaus ◽  
Rebecca J. Pearson ◽  
Ann M. Biehl ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Blood Glucose ◽  
Motor Function ◽  
Gastric Motility ◽  
Motor Nucleus ◽  
Gastric Tone ◽  
Antral Motility ◽  
Gastric Motor Function ◽  
Gastric Contractions

Our purposes were to 1) develop an animal model where intravenously (iv) administered d-glucose consistently inhibited antral motility, and 2) use this model to assess whether iv glucose acts to inhibit motility from a peripheral or a central nervous system site and to elucidate the factor(s) that determine(s) whether stomach motor function is sensitive to changes in blood glucose. Rats were anesthetized with α-chloralose-urethane, and antral motility was measured by a strain-gauge force transducer sutured to the antrum. In some cases, antral motility and gastric tone were measured by monitoring intragastric balloon pressure. Increases in blood glucose were produced by continuous iv infusion of 25% d-glucose at 2 ml/h. Inhibition of antral motility and gastric tone was observed when gastric contractions were induced by hypoglycemia (subcutaneously administered insulin, 2.5 IU/animal). In contrast, no inhibition of gastric motor function was observed when glucose infusion was tested on gastric contractions that were 1) spontaneously occurring, 2) evoked by iv administered bethanechol in vagotomized animals, and 3) evoked by the TRH analog RX77368, microinjected into the dorsal motor nucleus of the vagus. Using the model of insulin-induced hypoglycemia to increase gastric motor activity, we found that neither sectioning the hepatic branch of the vagus ( n = 5), nor treating animals with capsaicin to destroy sensory vagal afferent nerves ( n = 5) affected the ability of iv d-glucose to inhibit gastric motor function. Our results indicate that an important factor determining whether stomach motor function will be sensitive to changes in blood glucose is the method used to stimulate gastric contractions, and that the primary site of the inhibitory action of iv glucose on gastric motility is the central nervous system rather than the periphery.

Effect of CCK on proximal gastric motor function in humans

1998 ◽  
Vol 274 (5) ◽  
pp. G939-G944 ◽  
Author(s):  
Jan Willem A. Straathof ◽  
Banafsche Mearadji ◽  
Cornelis B. H. W. Lamers ◽  
Ad A. M. Masclee
Keyword(s):  
Motor Function ◽  
Physiological Role ◽  
Random Order ◽  
Saline Control ◽  
Abdominal Pressure ◽  
Continuous Intravenous Infusion ◽  
Visceral Perception ◽  
Visual Analog Scales ◽  
Abdominal Symptoms ◽  
Gastric Motor Function

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−1CCK, and 3) 1.0 IDU ⋅ kg−1 ⋅ h−1CCK. 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−1CCK 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−1CCK was significantly increased over saline (363 ± 44 vs. 195 ± 34 ml; P < 0.01) but not during 0.5 IDU ⋅ kg−1 ⋅ h−1CCK (195 ± 14 ml; not significant). During both isovolumetric and isobaric distensions, 1.0 IDU ⋅ kg−1 ⋅ h−1CCK significantly ( P < 0.05) increased proximal gastric compliance compared with saline. However, 0.5 IDU ⋅ kg−1 ⋅ h−1CCK had no significant effect on gastric compliance. During volume distensions, but not during fixed pressure distensions, 1.0 IDU ⋅ kg−1 ⋅ h−1CCK significantly ( P < 0.05) reduced visceral perception. These results suggest that in humans CCK may have a physiological role in regulating proximal gastric mechanics.

Effects of hyperglycaemia and hyperinsulinaemia on proximal gastric motor and sensory function in humans

2000 ◽  
Vol 99 (1) ◽  
pp. 37-46 ◽  
Author(s):  
A. S. VAN PETERSEN ◽  
M. K. VU ◽  
W. F. LAM ◽  
C. B. H. W. LAMERS ◽  
J. RINGERS ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Healthy Volunteers ◽  
Motor Function ◽  
Sensory Function ◽  
Symptom Perception ◽  
Gastric Function ◽  
Proximal Stomach ◽  
Acute Hyperglycaemia ◽  
Gastric Motor Function

During acute hyperglycaemia, gastric emptying is delayed and the compliance of the proximal stomach is increased significantly. It is not known whether the effect of hyperglycaemia on proximal gastric motor function in healthy volunteers results from endogenous hyperinsulinaemia. Therefore we studied the effects of acute hyperglycaemia and hyperinsulinaemia on proximal gastric function, measured using an electronic barostat. Eight healthy volunteers were studied on three separate occasions during: (a) normoglycaemia, (b) hyperglycaemic hyperinsulinaemic clamping, and (c) euglycaemic hyperinsulinaemic clamping. Gastric compliance was significantly (P < 0.01) increased during hyperglycaemia (44±5 ml/mmHg), and also during hyperinsulinaemia (38±4 ml/mmHg), compared with during normoglycaemia (31±3 ml/mmHg). During pressure distension, sensations of fullness were greater during hyperglycaemia and during hyperinsulinaemia compared with controls. At a set pressure of minimal distension pressure +2 mmHg, the intrabag volume was significantly higher during hyperglycaemia (292±36 ml; P < 0.05), but not during hyperinsulinaemia (161±35 ml), compared with during normoglycaemia (129±10 ml). Postprandial relaxation was significantly (P < 0.01) decreased during hyperglycaemia (93±64 ml) and hyperinsulinaemia (101±64 ml) compared with normoglycaemia (224±56 ml). Thus not only hyperglycaemia, but also hyperinsulinaemia, influences proximal gastric compliance, postprandial relaxation and symptom perception.

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