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Neurotrophin 3 (NT3) and its receptors are expressed throughout the gastrointestinal tract, especially in the enteric nervous system. However, little is known about the effects of NT3 on gastrointestinal motility. To investigate the effects of NT3 on gastric or colonic motility under baseline conditions, after subdiaphragmatic vagotomy and in a model of postoperative ileus. Sprague-Dawley rats were equipped with strain gauge transducers on the gastric or colonic wall. Motility was recorded for 30 min, followed by i.v. administration of NT3 and motility-recording for another 60 min. Experiments were performed on three consecutive days and separately in a postoperative ileus model. To evaluate a vagal pathway, experiments were also performed on vagotomized rats. NT3 inhibited gastric motility. This inhibitory effect was reduced by subdiaphragmatic vagotomy. Preoperative treatment with NT3 prolonged the postoperative gastric ileus compared to vehicle treatment. Colonic motility in the intact animal was unchanged by NT3, but was increased postoperatively. NT3 treatment inhibited gastric but not colonic motility. This inhibition of gastric motility seems to be partly mediated by the vagus nerve. NT3 aggravates gastric postoperative ileus but attenuates colonic postoperative ileus, which corresponds to the observed positive effects of NT3 on constipated patients.

Background: Nitric oxide (NO) is known to inhibit gastrointestinal motility. However, no detailed analysis of gastric, small intestinal and colonic motor effects, including effects on contraction frequency, has, as yet, been reported after NO inhibition in awake rats. We therefore investigated the effects of NO synthase inhibition on gastric, small intestinal and colonic motility in awake rats under baseline conditions and in a postoperative ileus model., Methods: In Sprague-Dawley rats, strain gauge transducers were sutured either to the gastric corpus, the small intestine or the colon. After 3 days, L-NMMA (NO synthase inhibitor), D-NMMA or vehicle was given i.v., while the motility was recorded continuously. In addition, postoperative gastric, small intestinal or colonic motility was investigated after L-NMMA or vehicle treatment prior to abdominal surgery. The motility index, the contraction amplitude, the area under the contraction amplitude and the contraction frequency were analysed., Results: L-NMMA decreased gastric motility to 60+/-8% for about 15 min, but continuously increased small intestinal motility to 221+/-22% and colonic motility to 125+/-7% compared to baseline (baseline=100%; p<0.01 for all comparisons). L-NMMA increased the contraction frequency throughout the gastrointestinal tract (stomach, 13+/-2%; small intestine, 8+/-1%; colon, 16+/-5%; p<0.01 vs. baseline for all comparisons). L-NMMA injection prior to surgery did not prohibit intraoperative inhibition of gastrointestinal motility, but did result in immediate recovery of gastric, small intestinal and colonic motility postoperatively (L-NMMA vs. vehicle, 0-60 min postoperatively; stomach, 90+/-9% vs. 53+/-3%; small intestine, 101+/-5% vs. 57+/-3%; colon, 134+/-6% vs. 60+/-5%; p<0.01 for all comparisons; no significant difference between preoperative baseline motility and L-NMMA treated rats postoperatively)., Conclusions: Under baseline conditions, endogenous NO inhibits small intestinal and colonic motility and gastric, small intestinal and colonic contraction frequency in awake rats. In the early postoperative period, endogenous NO is a major inhibitory component that seems to constitute the common final pathway of mediators and the neural pathways inhibiting gastrointestinal motility in rats.

Background: The barostat has been used to investigate gastrointestinal motility. No detailed technical evaluation to characterize the properties of this device for motility recordings has been reported. We, therefore, aimed to test the barostat in vitro under standardized conditions., Methods: Barostat and manometry recordings were performed using a combined catheter in a pressure chamber. Some of the experiments were made in pig sigmoid colon in order to mimic recordings in a hollow organ. Data are mean +/- SD., Results: Baseline changes of the bag volume under constant conditions were 3.9 +/- 2.0%. The bag volume increased by 4.5 +/- 1.1% with a temperature increase from 22 to 37 degrees C (p < 0.05). At external pressures above the bag operating pressure, the barostat bag collapsed, while only minimal volume reductions occurred at external pressures below the bag pressure. Barostat recordings of pressure events were delayed when compared with manometry and not linearly related to the pressure increases., Conclusion: The influence of temperature changes on barostat recordings is small. The volume decrease in the barostat bag is not linearly related to the external pressure increase and influenced by the operating pressure in the bag. This experimental study provides insight and caveats for those planning to use the barostat device for motility recordings of the gastrointestinal tract., (Copyright 2002 S. Karger AG, Basel)

Background: Gastrointestinal motility is frequently impaired after abdominal surgery. We investigated the effects of neostigmine on colonic motility in patients after colorectal surgery and in healthy volunteers., Methods: Colonic motility was recorded by a manometry/barostat system in 12 patients after left colonic or rectal resection during baseline and after the intravenous administration of increasing doses of neostigmine on postoperative days 1, 2, and 3. In addition, colonic motility was recorded in 7 healthy volunteers., Results: Neostigmine increased the colonic motility index. This increase was from 135 +/- 28 mm Hg/min at baseline to 574 +/- 219 mm Hg/min after administration of 5 microg/kg neostigmine on day 3 after surgery (mean +/- SEM, P <.05). In healthy volunteers, neostigmine at a dose of 5 microg/kg increased the colonic motility index from 184 +/- 73 to 446 +/- 114 mm Hg/min (P <.05). Barostat bag volumes decreased dose-dependently after neostigmine administration in patients as well as in volunteers, indicating an increase in colonic tone., Conclusions: Colonic motility and tone increased after neostigmine administration at a dose of 5 microg/kg in postoperative patients and in healthy volunteers. Neostigmine can be used to stimulate colonic motility after colorectal surgery and has a similar effect postoperatively as in healthy volunteers.

In a model to investigate postoperative gastrointestinal motility with strain gauge transducers in awake rats, we tested the effects of intraluminal capsaicin infusion into the cecum 2 days or 14 days prior to abdominal surgery. Acute infusion of capsaicin into the cecum for 30 minutes increased the gastric, small intestinal, and colonic motility index by up to 115%, 34%, and 59%, respectively, compared to vehicle infusion. Intraluminal capsaicin infusion 2 days prior to abdominal surgery significantly increased the intraoperative gastric and colonic motility index by 166% and 100%, respectively, compared to vehicle, but had no effect on small intestinal motility. The postoperative decrease in gastric or colonic motility was completely prevented by capsaicin pretreatment, representing a 73% and a 72% increase in the motility index during the first postoperative hour and a 40% and a 29% increase in the motility index during the second postoperative hour compared to vehicle, whereas the postoperative decrease in small intestinal motility was not altered by capsaicin pretreatment. In contrast, intraluminal capsaicin infusion 14 days prior to abdominal surgery had no effect on postoperative inhibition of gastrointestinal motility. Our results suggest that capsaicin-sensitive visceral afferent C-fibers, presumably of the submucosa, play an important role in mediating postoperative ileus. Intraluminal capsaicin does probably ablate these nerve fibers temporarily, with no systemic side effects observed with the use of the tail flick test as a measure of skin nociception.

Purpose: Colonic motility is crucial for the resolution of postoperative ileus. However, few data are available on postoperative colonic motility and no data on postoperative colonic tone. We aimed to characterize postoperative colonic tone and motility in patients., Methods: Nineteen patients were investigated with combined barostat and manometry recordings after left colonic surgery. During surgery a combined recording catheter was placed in the colon with two barostat bags and four manometry channels cephalad to the anastomosis. Recordings were performed twice daily from Day 1 to Day 3 after surgery., Results: Manometry showed an increasing colonic motility index, which was a mean (+/- standard error of the mean) of 37 +/- 5 mmHg/minute on Day 1, 87 +/- 19 mmHg/minute on Day 2, and 102 +/- 13 mmHg/minute on Day 3 (P < 0.05 for Day 1 vs. Day 2 and Day 2 vs. Day 3). Low barostat bag volumes indicating a high colonic tone were observed on Day 1 after surgery and increased subsequently (barostat bag I was 19 +/- 4, 32 +/- 6, and 32 +/- 6 ml; barostat bag II was 13 +/- 1, 19 +/- 3, and 22 +/- 5 ml on Days 1, 2, and 3, respectively; for both barostat bags P < 0.05 for Day 1 vs. Day 2 but not Day 2 vs. Day 3)., Conclusions: Colonic motility increased during the postoperative course. The low barostat bag volumes indicated a high colonic tone postoperatively which would correspond to a contracted rather than to a distended colon. High colonic tone postoperatively may be relevant for pharmacologic treatment of postoperative ileus.

Postoperative inhibition of colonic motility is a major contributor to postoperative ileus, but only limited information is available on its pathophysiology. We developed a model to record perioperative gastrointestinal motility in awake rats and investigated the effect of nitric oxide (NO) synthesis blockade on postoperative colonic ileus in rats. Rats were equipped with an i.v. catheter. Two strain gauge transducers were sutured to the colon, and the effects of NO synthesis blockade on postoperative colonic motility were investigated. NO synthesis blockade slightly increased baseline colonic motility. Abdominal surgery profoundly inhibited colonic motility. Blockade of NO synthesis did not prohibit intraoperative inhibition of colonic motility, but significantly hastened recovery of postoperative colonic ileus compared to vehicle. We established a model to record gastric, small intestinal and colonic motility in awake rats postoperatively. Laparotomy and short manipulation of the cecum produced a prolonged inhibition of colonic motility. Inhibition of NO synthesis improved recovery of postoperative colonic motility, indicating that NO partly mediates postoperative colonic ileus in rats.

Background: Postoperative ileus influences patients well-being, hospital stay, and health cost, and postoperative inhibition of colonic motility is a major contributor to postoperative ileus. Experimental models for investigating postoperative ileus are needed. In particular, recording of postoperative colonic motility in awake rats has not been described yet., Material and Methods: Gastric, small intestinal, and colonic motility were recorded with strain gauge transducers in awake rats, and the effects of anesthesia and abdominal surgery on gastrointestinal motility were investigated., Results: Ether anesthesia increased gastric motility and inhibited small intestinal motility, while enflurane anesthesia had only minor effects on gastrointestinal motility. Abdominal surgery inhibited gastric, small intestinal, and colonic motility, and a detailed analysis of gastrointestinal motility in our postoperative ileus model is given., Conclusions: We established a model to record gastric, small intestinal, and colonic motility in awake rats postoperatively. We could demonstrate that enflurane anesthesia had little effect on gastrointestinal motility, while laparotomy and short manipulation of the cecum produced a prolonged inhibition of gastrointestinal motility. Our model could be used to investigate postoperative ileus, particularly of the colon, in awake rats.

Carbohydrates are a component of chyme that initiate feedback control of gastric emptying. The aim of the study was to investigate the mechanism by which sensors in the intestine are activated by carbohydrate to initiate intestinal feedback of gastric motor function. Intestinal perfusion with D-glucose inhibited gastric motility in awake rats. This response was reproduced by 3-O-methyl glucose, a non-metabolizable analogue of glucose that is absorbed by the Na(+)-glucose co-transporter, but not by 2-deoxy-D-glucose, and was attenuated by perfusion of the intestine with phloridzin, a competitive blocker of the Na(+)-glucose co-transporter. Feeding a high carbohydrate diet to increase the number of co-transporters reduced the response to intestinal glucose. It was concluded that activation of sensors to initiate feedback inhibition of gastric motility may be dependent either on rapid accumulation of glucose within epithelial cells or on activation of the Na(+)-glucose co-transporter.

Objective: The object of this study was to investigate the mechanisms of postoperative gastric ileus in an experimental model of abdominal surgery in anesthetized rats., Summary Background Data: Sensory neurons partly mediate postoperative gastric ileus. Among other neuropeptides, sensory neurons contain calcitonin gene-related peptide (CGRP) and release CGRP in response to noxious stimulation. Because CGRP inhibits gastric motility, it was hypothesized that abdominal surgery stimulates sensory neurons, which then releases CGRP, thereby inhibiting gastric motility., Methods: Postoperative ileus was induced by abdominal surgery. Gastric corpus motility was measured by an intragastric catheter. CGRP action was blocked by CGRP immunoneutralization or by a CGRP receptor antagonist. Spinal sensory neurons were ablated by application of a sensory neurotoxin (capsaicin) to the celiac and superior mesenteric ganglia., Results: Abdominal surgery decreased gastric corpus motility in the first 5 minutes after abdominal surgery by 59 +/- 5% and by 24 +/- 4% during the 1st postoperative hour. Capsaicin pretreatment of the celiac and superior mesenteric ganglia, CGRP immunoneutralization, or CGRP receptor antagonism reversed the postoperative decrease in gastric corpus motility during the 1st postoperative hour by 50%, 100%, and 59%, respectively., Conclusions: These data indicate that spinal sensory neurons and CGRP partly mediate postoperative gastric ileus. CGRP may be released from spinal sensory neuron terminals in the celiac and superior mesenteric ganglia as part of an extraspinal intestinogastric inhibitory reflex activated by abdominal surgery.

Neurotrophin 3 (NT3) and its receptors are expressed throughout the gastrointestinal tract, especially in the enteric nervous system. However, little is known about the effects of NT3 on gastrointestinal motility. To investigate the effects of NT3 on gastric or colonic motility under baseline conditions, after subdiaphragmatic vagotomy and in a model of postoperative ileus. Sprague–Dawley rats were equipped with strain gauge transducers on the gastric or colonic wall. Motility was recorded for 30 min, followed by i.v. administration of NT3 and motility-recording for another 60 min. Experiments were performed on three consecutive days and separately in a postoperative ileus model. To evaluate a vagal pathway, experiments were also performed on vagotomized rats. NT3 inhibited gastric motility. This inhibitory effect was reduced by subdiaphragmatic vagotomy. Preoperative treatment with NT3 prolonged the postoperative gastric ileus compared to vehicle treatment. Colonic motility in the intact animal was unchanged by NT3, but was increased postoperatively. NT3 treatment inhibited gastric but not colonic motility. This inhibition of gastric motility seems to be partly mediated by the vagus nerve. NT3 aggravates gastric postoperative ileus but attenuates colonic postoperative ileus, which corresponds to the observed positive effects of NT3 on constipated patients. [ABSTRACT FROM AUTHOR]

A correction to the article "Effects of Neurotrophin 3 on Gastric and Colonic Motility in Awake Rats," by M. A. Kueper, T. Meile, T. T. Zittel, A. Konigsrainer and J. Glatzle, is presented.