Pentagastrin induced motility pattern in the human upper gastrointestinal tract is reversed by proglumide

The effects of pentagastrin and the putative gastrin antagonist proglumide on interdigestive motility of the upper small bowel were studied in a randomised double blind study in 10 healthy human volunteers. Intraluminal pressures were recorded manometrically in the duodenum and jejunum for five hours. Sixty minutes after starting a pentagastrin infusion (0.15 micrograms/kg/h) either placebo or proglumide was infused intravenously. Pentagastrin converted the normal interdigestive motility to irregular motor activity, while proglumide restored the periodic fasted pattern. We conclude that gastrin is a likely candidate involved in the conversion of the fasted to the fed motility pattern in the human upper gut.     

Effect of painless rectal distension on gastrointestinal transit of solid meal

The effect of painless intermittent rectal distension on the rate at which a standard meal passes through the stomach and small intestine was investigated in normal volunteers using noninvasive techniques. Rectal distension significantly retarded the entry of the head of the meal into the cecum and the emptying of the meal from the stomach, although it had no significant effect on basal gastric acid secretion. After administration of the H ₂ -receptor antagonist, ranitidine, there was no significant effect of rectal distension on gastric emptying, but the delay in small bowel transit time induced by rectal distension remained. These data indicate that events occurring in the rectum may influence the function of more proximal regions of the gut.     

上消化道动力临床检测技术

上消化道动力障碍性疾病是消化系统的常见病 ,掌握消化道运动功能检测技术将有助于该类疾病的诊断及疗效的判定。以下介绍几种常用的检测技术。1　食管运动功能检测1.1　食管测压技术　是判定有否食管运动功能紊乱的基本方法 ,其主要适应证为典型或不典型食管症状如非进行性吞咽困难、烧心、反胃等 ,经有关检查未发现器质性病变者。目前主要有液压灌注导管外传感器法、腔内微型压力传感器法等 ,后者属远侧型传感压力记录系统 ,由传感器直接测量腔内压力 ,主要有电磁压力传感器和半导体压力传感器 ,该仪器制作成本高 ,且易于损坏 ,故限制了临…     

Anal and rectal motility responses to distension of the urinary bladder in man

Recto-anal motility response to bladder distension was studied under general anaesthesia in 12 patients undergoing intestinal resection for Crohn's disease of the small intestine or colonic cancer. The effect of epidural anaesthesia on anal tone and on the motility response to bladder distension was studied in six of these patients. An anal pressure increase on bladder distension was observed in all individuals. No motility response was noted in the rectum. The anal pressure response to bladder distension was abolished by epidural anaesthesia. It was concluded that anal pressure in man under general anaesthesia was tonically influenced by the thoracolumbar sympathetic outflow. An excitatory vesico-anal reflex was demonstrated. It appears as this reflex is mediated via the spinal cord.

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Résumé La réponse motrice recto-anale à une distension de la vessie a été étudiée sous anesthésie générale chez 12 patients devant subir des résection intestinales pour une maladie de Crohn ou un cancer colique. L'effect d'une anesthésie épidurale sur le tonus anal et sur la réponse motrice à une distension vésicale a été étudiée chez 6 de ces patients. Une augmentation de la pression anale secondaire à la distension vésicale a été observée chez tous les sujets. Aucune réponse motrice n'a été observée au niveau du rectum. L'anesthésie épidurale abolit la réponse au niveau du sphincter à la distension vésicale. On conclut de cette étude que la pression anale chez l'homme sous anesthésie générale est influencée par le système sympathique thoraco-lombaire. Un réflexe d'excitation vésico-anale a été mis en évidence. Ce réflexe passe la moëlle épinière.

     

Intra-gastric triacetin alters upper gastrointestinal motility in conscious dogs

AIM:To examine the effect of intra-gastric triacetin on both upper gastrointestinal motility and proximal gastric tone in conscious dogs.METHODS:Three beagle dogs under sedation were surgically implanted with gastrocutaneous fistula in the gastric body and force transducers in the gastric antrum and duodenum.Beginning at week-2 after insertion,the animals were either fasted for 24 h or fed a liquid meal 2-3 h before the experiment.With the animals fully conscious,a polyethylene bag was inserted into the proximal stomach through the gastrocutaneous fistula,followed by 15 min of air inflation(minimal distending pressure of+2 mmHg)and then 20 mL of a low-,mid-or high-concentration triacetin solution(0.5%,1.0%and 2.0%)or warm water(vehicle control).The proximal stomach receptive volume and gastric antral and duodenal contractions were measured over 10 min.The experiment was repeated twice per week over several months,with each animal receiving at least one infusion of the various triacetin solutions and the vehicle at different times.Intergroup differences were assessed by ANOVA and Bonferroni-Dunn post-hoc testing.RESULTS:Intra-gastric infusion of mid-and high-concentration triacetin induced an increase in the proximal stomach receptive volume,and the average increase induced by the high-concentration at 0-4 min after infusion was significantly greater than that induced by the vehicle control(62.4±9.8 vs 18.4±4.7,P<0.01).The mid-and high-concentration triacetin also produced a temporary inhibition of the gastric antral contractions at 2 min after infusions;however,only the fasted group showed triacetin-induced antral contractile inhibition that was significantly greater than that in the vehicle control group(P<0.05).In addition,only the fasted group showed a high-concentration triacetininduced increase in duodenal contractions at 9-10 min that was significantly different from that in the vehicle control group(P<0.05).CONCLUSION:Intra-gastric infusion of 1.0%-2.0%triacetin delays gastric emptying by increasing proximal stomach receptive volume,temporarily inhibiting gastric antral contractions and facilitating duodenal contractions.     

Genetic contribution to motility disorders of the upper gastrointestinal tract

Motility disorders of the upper gastrointestinal tract encompass a wide range of different diseases. Esophageal achalasia and functional dyspepsia are representative disorders of impaired motility of the esophagus and stomach, respectively. In spite of their variable prevalence, what both diseases have in common is poor knowledge of their etiology and pathophysiology. There is some evidence showing that there is a genetic predisposition towards these diseases, especially for achalasia. Many authors have investigated the possible genes involved, stressing the autoimmune or the neurological hypothesis, but there is very little data available. Similarly, studies supporting a post-infective etiology, based on an altered immune response in susceptible individuals, need to be validated. Further association studies can help to explain this complex picture and find new therapeutic targets. The aim of this review is to summarize current knowledge of genetics in motility disorders of the upper gastrointestinal tract, addressing how genetics contributes to the development of achalasia and functional dyspepsia respectively.     

Actions of thyrotropin-releasing hormone on gastrointestinal functions in man. III. Inhibition of gastric motility in response to distension.

The intragastric pressure/volume relationship has been measured in six healthy volunteers. Increased gastric motility was achieved by gastric distension, by stepwise increasing the volume from 0--600 ml. When thyrotropin-releasing hormone (TRH), 0.04 mg/h, was infused concomitantly in the individuals, gastric motility was significantly inhibited (p less than 0.05) and, with 1 mh/h of TRH, nearly abolished compared with the saline control test. The basal pressure was unaffected at 0.04 mg/h, whereas a significant rise was seen after 1 mg/h of TRH (p less than 0.05) compared with the control test. In three of the subjects the effect of rapid injection of TRH (0.2 mg), followed by infusion of TRH (0.6 mg/h), on the stimulated gastric motility was analysed. After the injection of TRH, almost no motor activity was observed during the 15-min observation period. It is concluded that TRH has a potent inhibiting effect on gastric motility, and the possible physiological role of TRH in the gastric regulation in man is discussed.     

Effects of famotidine on upper gastrointestinal motility in patients with progressive systemic sclerosis.

The effects of famotidine on human upper gastrointestinal motility were investigated, together with the relationship of gastric alkalinization and serum gastrin levels to changes produced by famotidine. Intravenous famotidine (20 mg), at a dose level in which an inhibitory effect on acetylcholinesterase activity is not recognized, was given to 13 patients with progressive systemic sclerosis but no other disorders. Gastric phasic motor activity was not changed significantly, but the lower esophageal sphincter pressure was elevated significantly in comparison with 15 controls given physiological saline, even when gastric phasic motor activity was taken into consideration. Gastric alkalinization with 7% sodium bicarbonate did not significantly increase the sphincter pressure in all 7 subjects so treated. No significant correlation was recognized between the serum gastrin level, the lower esophageal sphincter pressure, and the gastric motility index in any of the 3 groups. It was, therefore, concluded that intravenous administration of famotidine affected upper gastrointestinal motility, especially the lower esophageal sphincter pressure, through an as yet unknown mechanism other than inhibition of acetylcholinesterase activity, gastric alkalinization, or elevation of serum gastrin levels.     

Effect of cyclical unipolar depression on upper gastrointestinal motility and sleep

Cyclic 48-h unipolar depression is a rare form of recurrent affective disorder. We studied a single patient to determine (a) if there is an association between psychiatric status and migrating motor complex activity; and (b) if phase III of the migrating motor complex is in phase with rapid eye movement sleep in depression. There was marked reduction in phase III of the migrating motor complex during the depressed (n = 7) compared with the euthymic phase (n = 13), and a lack of coherence between phase III migrating motor complex activity and sleep stages in both depressed and nondepressed phases. The depressed state may be associated with altered upper gastrointestinal motor function.     

Modulation of human upper intestinal nutrient transit by a beta adrenoreceptor mediated pathway.

To explore the role played by beta adrenoreceptor mediated pathways on human upper gut function a series of studies were conducted into the effects of beta adrenoreceptor agonists and antagonists on orocaecal and duodenocaecal transit and on antral and duodenal motor activity. Under control conditions orocaecal transit was consistent within individuals (mean coefficient of variation (18.0%) but varied widely between individuals (median transit 63 minutes, range 33-164). Prior administration of the non-selective beta adrenergic antagonist propranolol consistently hastened orocaecal transit (median transit 51:25-93, v control p < 0.005). The selective beta-1 antagonist, atenolol, also hastened transit (median transit 50:35-93 minutes, v control p < 0.01). The magnitude of an individual's response to beta blockade correlated closely with the orocaecal transit (Tau = 0.54, p < 0.01). Duodenocaecal transit was also hastened by propranolol from control values of 66:45-107 minutes to 50:16-62 minutes, p < 0.025). In contrast neither duodenal nor antral motility were consistently altered by beta blockade. The beta adrenoreceptor agonist, isoprenaline, delayed both orocaecal transient (97:55-178 minutes, v control p < 0.005) and also duodenocaecal transit (160:45-215 minutes, v 73:40-133) (p < 0.025). Isoprenaline also reduced antral motility by an effect which appeared to occur predominantly through a reduction in contraction amplitude (from a median amplitude of 27:5.39 mm Hg to 14:3-24 mm Hg, p < 0.03) rather than an effect on the interval between contractions. No effect on either amplitude or frequency of duodenal motor activity was observed. A beta adrenoreceptor mediated pathway thus appears to exert a biologically relevant effect on gut function not only under conditions of sympathetic stimulation, but also at rest when a basal beta adrenergic tone appears to influence the speed of nutrient transit through the human upper gut.     

Perturbation of upper gastrointestinal transit and antroduodenal motility by experimentally applied stress: the role of beta-adrenoreceptor mediated pathways.

A series of three experiments were performed on healthy adult volunteers to investigate the possible role played by beta-adrenoreceptor mediated pathways in the disturbance of human upper intestinal motor function by hand immersion in cold water. In the first experiment, (an extended pilot study on one individual), orocaecal transit of a standard meal was measured on 36 occasions with and without cold water stimulation and with and without a series of alpha and beta blocking drugs. Cold water stimulation consistently delayed transit in this individual, an effect which was attenuated by prior beta-blockade. In a double blind trial of the effect of beta-blocker atenolol v placebo on transit in nine individuals, a consistent reduction in the cold water induced transit delay was observed (p less than 0.01) independent of any direct effect of beta-blockade. In the third experiment seven individuals underwent repeated studies of antroduodenal pressure activity comparing the effects of cold and warm water stimulation with and without beta blockade to determine whether the observed transit effect could be related to an action on gastrointestinal motility. Cold water stimulation reduced antroduodenal motility, but no consistent effects of previous beta blockade were noted. These studies indicate the presence of a beta-adrenoreceptor mediated pathway in the cold water induced delay of orocaecal transit but not in the inhibition of gastroduodenal motility. Further studies are indicated to determine the site and mode of action of this transit effect more precisely.     

Perturbation of upper gastrointestinal function by cold stress.

To study the effects of stressful stimulus (cold pain) upon postprandial gastric, duodenal, and pancreatic function, nine healthy adult volunteers were intubated and then given two identical liquid meals, (199 cal (789 KJ) 240 ml), each being ingested during a period of irregular fasting gastroduodenal motility. Ten minutes after each meal the subjects received, in randomised order, either a test or control stimulus. The test stimulus consisted of repeated one minute immersions of a hand into ice water, with 15 seconds recovery between immersions, for a total of 20 minutes, while for the control, water at 37 degrees C was used. Serial samples of gastric and duodenal contents allowed estimation of changes in gastric emptying and acid secretion, together with pancreatic trypsin output, by a double marker perfusion technique. Measurements of blood pressure, pulse, and finger temperature acted as extra-intestinal indices of autonomic response to the stimuli. Cold pain significantly delayed gastric emptying and produced a biphasic alteration in both gastric secretion and pancreatic trypsin output, with an initial reduction during the response to the stress followed by an increase during the post-stress period. Our findings show that the normal postprandial function of the upper gut can be measurably disturbed by a stressful stimulus. The coincidence of these disturbances with other extra-intestinal autonomic changes suggests that they are a further manifestation of the somatic response to a stress.     

Clinical and upper gastrointestinal motility features in systemic sclerosis and related disorders

Objective: The aim of this study was to characterize the clinical and motility findings in 62 patients with systemic sclerosis or related disorders referred for evaluation of upper gastrointestinal (GI) symptoms.
Methods: Methods included retrospective clinical record review and quantitation of esophageal, LES antral, and duodenal motility (3 h fasting, 2 h fed) were compared with results of 10 symptomatic patients with normal gastric emptying.
Results: A total of 46 patients had systemic sclerosis, eight mixed connective tissue disease, and eight polymyositis-systemic sclerosis overlap; systemic manifestations were almost invariably present. GI symptoms were: heartburn (77%), nausea/vomiting (58%), dysphagia (61%), diarrhea (53%), constipation (31%), and fecal incontinence (13%). Anatomical studies showed esophageal erosions or GERD (53%), aperistalsis (34%), stricture (29%), and Barrett's metaplasia (16%); megaduodenum, small bowel dilation, or diverticulae (42%); and pneumatosis intestinalis (8%). A total of 36 patients underwent esophageal and 26 esophagogastrointestinal manometry. Postprandial antral motility index was abnormal in 22 of 26; amplitudes and frequency in the antrum (34 ± 3 mm Hg and 0.6 ± 0.1/min, respectively) and duodenum (7.3 ± 0.9 mm Hg and 1.8 ± 0.5/min) were significantly lower than controls (   p < 0.05  ).
Conclusion: In patients with GI symptoms associated with systemic sclerosis and related disorders, the amplitude and frequency of intestinal contractions are typically <10 mm Hg and <2/min. Antral amplitude is low (<40 mm Hg) when antral hypomotility is observed.     

Activation of human adenylate cyclase in the upper gastrointestinal tract by vasoactive intestinal polypeptide.

The effects of various polypeptide hormones known to inhibit gastric acid secretion were tested on the adenylate cyclase system in human gastric and duodenal mucosal homogenates. Glucagon and secretin failed to stimulate the enzyme system in the stomach. The latter hormone produced a small but significant activation of the duodenal cyclase. The vasoactive intestinal polypeptide (VIP), however, induced a dose-dependent increase of enzyme activity throughout the stomach and the duodenum. Maximal effects (1.8 to 3.0-fold increase) were observed at a VIP-concentration of about 10 microgram per ml. Because the entire physiological role of VIP in gastric function has not been defined, ipt cannot be discerned whether the VIP-stimulated adenylate cyclase is linked to inhibition of gastric acid secretion or to another as yet unrecognized effect of this hormone in human gastric function.     

Effects of famotidine on upper gastrointestinal motility in patients with progressive systemic sclerosis

The effects of famotidine on human upper gastrointestinal motility were investigated, together with the relationship of gastric alkalinization and serum gastrin levels to changes produced by famotidine. Intravenous famotidine (20 mg), at a dose level in which an inhibitory effect on acetylcholinesterase activity is not recognized, was given to 13 patients with progressive systemic sclerosis but no other disorders. Gastric phasic motor activity was not changed significantly, but the lower esophageal sphincter pressure was elevated significantly in comparison with 15 controls given physiological saline, even when gastric phasic motor activity was taken into consideration. Gastric alkalinization with 7% sodium bicarbonate did not significantly increase the sphincter pressure in all 7 subjects so treated. No significant correlation was recognized between the serum gastrin level, the lower esophageal sphincter pressure, and the gastric motility index in any of the 3 groups. It was, therefore, concluded that intravenous administration of famotidine affected upper gastrointestinal motility, especially the lower esophageal sphincter pressure, through an as yet unknown mechanism other than inhibition of acetylcholinesterase activity, gastric alkalinization, or elevation of serum gastrin levels.