Hanson, Russell B.

The effects of pharmacological modulation of adrenergic receptors on colonic motor and sensory function are unclear. We studied 40 healthy volunteers in a single-blind design; 12 received saline, and the remaining 28 received either clonidine, yohimbine, phenylephrine, or ritodrine. A barostat-manometric assembly in the left colon recorded drug effects on fasting and postprandial motor function, compliance, and sensation in response to standardized phasic balloon distensions delivered in random order. Clonidine reduced and yohimbine increased fasting, but not postprandial tone, by 63.2 ± 22.3% and 24.8 ± 8.8% (SE), respectively. Clonidine tended to reduce fasting phasic activity in the descending and sigmoid colon. A power exponential model provided the best fit to the compliance curve. Clonidine significantly increased colonic compliance. Clonidine reduced and yohimbine increased colonic perception of pain but not gas sensation during distension. Phenylephrine and ritodrine did not influence colonic motor or sensory function in the present studies. Thus α2-receptors modulate fasting colonic tone and compliance and alter perception of pain but not gas during mechanical stimulation of the colon.

The hypothesis was that orally moving pacesetter potentials distal to a site of jejunal transection and anastomosis would slow transit through jejunum containing them and that reoperation with excision of bowel containing these pacesetter potentials would restore transit to the control. In six conscious dogs with jejunal serosal electrodes for recording myoelectric activity and a jejunal perfusion/aspiration catheter for measuring transit, jejunal pacesetter potential frequency decreased distal to a midjejunal transection and anastomosis from 18.7 +/- 0.3 (SE) cycles/min (cpm) proximal to the site to 14.4 +/- 0.6 cpm distal to the site (P < 0.05). In addition, orally propagating pacesetter potentials occurred > 25% of the time in a 37 +/- 7 cm length of bowel distal to the site during fasting and after feeding. Transit through the segment with the orally moving pacesetter potentials was slowed during feeding (half time before and after transection, 7.7 +/- 1.1 and 13 +/- 2.0 min, respectively, P < 0.05). Resection of the segment with the abnormal pacesetter potentials shortened the length of bowel containing them to 24 +/- 2 cm (P > 0.05) and restored transit to the control. In conclusion, orally moving pacesetter potentials distal to a canine jejunal transection and anastomosis slowed transit through the segment of bowel containing them. Resection of the segment restored transit to the control.

The aims of this study were to determine the effects of duodenal and jejunoileal nutrient infusions on small intestinal motor patterns and intestinal contractions in neurally intact and neurally isolated small bowel. Fifteen dogs were prepared with duodenal and jejunal infusion and manometry catheters and a diverting jejunal cannula. Ten of the dogs underwent in situ neural isolation of the jejunoileum. A mixed nutrient meal (0.5 kcal/ml) was infused into the duodenum or jejunum at 3 ml/min for 5 h. Control experiments involved infusion of a balanced salt solution. Manometric data collected on-line to a microcomputer were analyzed for direction, distance, and velocity of spread of single pressure waves (SPW) and clustered contractions. Isolated duodenal and jejunoileal nutrient infusions inhibited the fasting motor pattern in neurally intact and neurally isolated small bowel. Motor activity (motility index) increased slightly during nutrient infusion within groups, but there were few differences between groups. Neither neural isolation nor nutrient infusion had a consistent effect on spread of SPW or migration of clustered contractions. Isolated duodenal and jejunoileal nutrient infusions in the dog inhibit fasting motor patterns and increase motor activity slightly but have little effect on characteristics of individual and clustered contractions. Extrinsic innervation to the jejunoileum or intrinsic neural continuity of the jejunum with the duodenum had little effect on single or grouped contractions. Although the changes in motor activity demonstrated in this study appear small, alterations in intestinal transit and absorption may still occur and may be of importance physiologically.

Our aims were to assess the role of adrenergic modulation in the hyperventilation-induced increase in colonic tone. Of 40 healthy volunteers, 12 received placebo (saline) and the remaining 28 received either clonidine, yohimbine, phenylephrine, or ritodrine. Time-frequency mapping of heart rate based on Wigner distribution assessed variations in parasympathetic and sympathetic activity during hyperventilation. Tone in the descending colon was recorded by a barostat balloon before, during, and after 5 min of hyperventilation. Heart rate spectral analysis suggested diminished sympathetic and vagal activity during hyperventilation and increased sympathetic and vagal activity after hyperventilation. Adrenergic agents influenced ( P = 0.01) the tonic response after, but not during, hyperventilation. Yohimbine reduced the increment in colonic tone after hyperventilation compared with saline ( P < 0.05) and clonidine ( P = 0.002); phenylephrine and ritodrine had no effects. Different mechanisms modulate the increase in colonic tone during and after hyperventilation. Yohimbine attenuates the increase in colonic tone after hyperventilation probably by enhancing inhibitory sympathetic input to the colon.

Our aim was to determine the effect of in situ neural isolation of the jejunoileum (extrinsic denervation and disruption of enteric neural continuity with the duodenum) on the spread of single pressure waves (SPW) and clustered contractions (CC) in response to increasing rates of isolated duodenal and jejunoileal nonnutrient infusions. Ten dogs were prepared with duodenal and jejunal infusion and manometry catheters and a diverting proximal jejunal cannula. Five of the dogs also underwent in situ neural isolation of the entire jejuno- ileum A noncaloric solution was infused at 0-15 ml/min into proximal duodenum or jejunum while manometric data were collected. Alterations in direction, distance, and velocity of spread of SPW and CC with increasing rates of intestinal infusion were analyzed by linear regression of responses to increasing infusion rates. Neural isolation of the jejunoileum did not markedly alter characteristics of duodenal or jejunal SPW or CC under conditions of no intestinal infusion. After neural isolation of jejunoileum, increasing rates of jejunal infusion decreased both the proportion and distance of antegrade spread of SPW in duodenum. These findings suggest that extrinsic innervation to the jejunoileum and enteric neural continuity with the duodenum do not regulate jejunal SPW or CC. Increasing rates of nonnutrient intestinal infusions do not alter local motor patterns in the innervated or neurally isolated jejunum, but after neural isolation of the jejunoileum, these infusions do alter characteristics of duodenal SPW by mechanisms independent of neural pathways.

We describe here further observations on a novel motor phenomenon that can be recorded regularly from the canine ileum in the late postprandial period, i.e., when residue of a meal reaches the distal small bowel. We reported before that this unique pattern of motility consisted of intraluminal pressure waves at a frequency (20-24/min) much greater than that of the ileal slow wave. In the current experiments, we document that these intraluminal pressure waves coincide with contraction of the circular muscle layer, as recorded from serosal strain gauges. However, the cellular origin and propagation of these contractile events are still unclear. By studying dogs with ileal loops and those with an intact bowel, we conclude that this is a local response of the ileum to the arrival of nutrients in its lumen and that it is under cholinergic control. This report supports the concept that the ileum may be particularly sensitive to its local intraluminal environment.

Our hypothesis was that the direction of liquid transit through the canine jejunum is determined by the direction that single jejunal pressure waves spread, while the direction of solid transit depends on the direction of spread of both single waves and clustered waves. In six dogs, 80-cm jejunal Vella loops were made and fitted with manometric catheters and serosal electrodes. After recovery, transit of liquids (Ringer lactate) and solids (2.4-mm nylon spheres) placed into the center of the loop was determined in the conscious animals while pacing the loop in a forward direction or in a backward direction. Under fasting and fed conditions, single pressure waves followed the direction of pacing, while the direction of migration of clustered waves was not determined by the direction of pacing. Liquid transit always followed the direction of single pressure waves. In contrast, solids moved distally regardless of the direction of pacing, except when liquids were also present in the lumen, in which case solids moved in the same direction as the single pressure waves.

We report here a novel motor phenomenon that we recorded from the canine terminal ileum in the postprandial period. In chronic models that allowed us to monitor myoelectrical activity and intraluminal pressure from the jejunum and distal ileum, we regularly saw in the ileum, but not in the jejunum, a rhythmic sequence of intraluminal pressure waves at a frequency of 19-24 cycles/min. This unusual motor pattern was rarely seen in the first 2 h after food and was essentially absent during fasting; it appeared reproducibly 1-4 h after food, at the time when chyme reached the ileum. The phenomenon was accompanied by spike bursts that were usually at the same rapid, rhythmic frequency, but the rate of the ileal slow wave persisted at the preprandial level (13-15/min). These findings further exemplify differences in the regulation of the motility between jejunum and ileum; moreover, the phenomenon highlights the capacity of the distal small intestine to response specifically to the nature of its luminal contents. This reaction of the ileum to the arrival of dietary residues is deserving of further study in the evaluation of the small bowel's response to a meal.

Our aim was to measure axial forces in the stomach and to evaluate their relation to circumferential contractions of the gastric walls and the emptying of gastric content. We used a combination of simultaneous radioscintigraphy, gastroduodenal manometry, and an axial force transducer with an inflatable 2-ml balloon fluoroscopically placed in the antrum. In vitro studies demonstrated that the axial force transducer records only antegrade forces along the longitudinal axis of this probe in an intensity-dependent manner. In vivo studies were performed in five healthy subjects for at least 3 h after ingestion of radiolabeled meals. When administered separately, the emptying of liquids or solids from the stomach is associated with generation of antral axial forces and coincident phasic pressure activity; however, almost 20% (average) of gastric axial forces during emptying of liquids or solids are unassociated with proximal or distal antral pressure activity ("isolated" forces). High amplitude antral axial forces and pressures occur during both lag and postlag emptying phases. During emptying of liquids, there is a trend for axial forces to be coincident more often with proximal than with distal antral pressure activity and vice versa for the emptying of solids (P = 0.015). These data suggest that when placed in the antrum, the transducer can semiquantitatively record axial forces during gastric emptying. By combining these observations with the data from in vitro studies, it appears that axial forces predominantly result from traction on the balloon by the longitudinal vector resulting from circumferential gastric contractions. The combination of radioscintigraphy and measurement of antral axial forces is a promising method to evaluate mechanical forces involved in the emptying of the human stomach.

Background The pathophysiological mechanisms in non-ulcer dyspepsia are incompletely understood. Aims To compare gastric motor and sensory functions in Helicobacter pylori positive or negative patients with non-ulcer dyspepsia. Patients Seventeen patients with non-ulcer dyspepsia and 16 asymptomatic controls. Methods The following were evaluated: gastrointestinal symptoms; gastric emptying and orocaecal transit of solids; abdominal vagal function; gastric compliance; fasting and postprandial gastric tone and phasic contractions; symptoms during ingestion of cold water and during the distension of an intragastric bag; and somatic sensitivity and personality profile (Minnesota Multiphasic Personality Inventory, MMPI). Results Gastric accommodation was reduced in H pylori negative dyspeptics relative to controls; the degree of accommodation was unrelated to H pylori status in dyspeptics. Increased postprandial gastric sensation was more frequent among H pylori positive patients (4/5 H pylori positive versus 4/12 H pylori negative patients). Intragastric meal distribution and orocaecal transit were normal; gastric emptying at four hours was abnormal in 4/17 patients. Vagal dysfunction was rare. Eight of 17 patients had somatisation or depression on MMPI. Conclusion Impaired gastric accommodation is frequent in non-ulcer dyspepsia and seems to be unrelated to vagal efferent dysfunction. H pylori infection does not seem to influence gastric accommodation, but is associated with heightened sensitivity in dyspeptics. Therapeutic approaches that restore normal postprandial accommodation and gastric sensitivity should be tested in non-ulcer dyspepsia.