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At least 793 records · Page 44Linked to original sources
PubMed1992

Effect of early feeding on maturation of the preterm infant's small intestine.

To determine the response of the preterm infant's intestine to entire feedings at different postnatal ages, we recorded results of manometry of the gastroduodenum and determined fasting plasma concentrations of gastrin, gastric inhibitory peptide, neurotensin, and peptide YY three times in each of two groups: 27 preterm infants were randomly assigned to receive hypocaloric enteral nutrition on postnatal days 3 to 5 (early feeding) or on days 10 to 14 (late feeding). Initial observations (study 1) were performed by the fifth postnatal day; study 2 was performed on days 10 to 14, and study 3 on days 24 to 28. Early-fed infants received hypocaloric feedings immediately after study 1; late-fed infants did not receive enteral feedings until the completion of study 2. Although motor activity and fasting gastrointestinal peptide concentrations did not differ between groups at study 1, at study 2 early-fed infants had significantly more mature motor patterns than did babies not being fed. Early-fed infants also had significantly higher plasma concentrations of gastrin and gastric inhibitory peptide than did late-fed infants; neurotensin and peptide YY values were similar in both groups. By the time of study 3, when late-fed infants had also received enteral feedings, gut development was not different in the two groups. However, early-fed infants were able to tolerate full oral nutrition sooner, had fewer days of feeding intolerance, and had shorter hospital stays. Thus the provision of early hypocaloric nutrition was associated with earlier nutrition of preterm infants' intestinal function and resulted in improved feeding tolerance. These findings support the use of early feedings in preterm infants.

Energy Intake↗
PubMed2004

Limitations of implantable, miniature ultrasonic transducers to measure wall movement in the canine jejunum.

BACKGROUND: We used implantable miniature ultrasonic transducers to measure longitudinal distance, circumference, and wall thickness dynamically in vivo in canine jejunum. We hoped to differentiate circular from longitudinal smooth muscle contractions and to correlate physical measurements of change in distance within the jejunal wall with intraluminal manometry. MATERIALS AND METHODS: In acute experiments at the time of celiotomy, longitudinal distances, circumferences, and wall thickness were measured directly and by ultrasonic transducers sewn to serosa and mucosa. Measurements were obtained with the intestine empty and after distention with air, water, or semisolid slurry. In chronic in vivo experiments in conscious dogs with indwelling ultrasonic transducers and intraluminal manometers, sonometric dimensions were correlated with manometric recordings. In acute experiments, sonometric measurements were similar to direct measurements. In chronic experiments in vivo, smallest ultrasonometric measurements of circumferences of the jejunum correlated in a phase-locked temporal manner with both highest intraluminal pressures and greatest wall thickness. RESULTS: Longitudinal distances increased during decreases in circumference. Distances orad to the site maximal intraluminal pressure peaked at 0.58 +/- 0.04 s ( x +/- SEM) before, and those aborad to this point 0.42 +/- 0.04 s after attaining minimum circumferences. CONCLUSIONS: Ultrasonic crystals can monitor geometric changes in the bowel wall with certain limitations, especially when obtained in vivo. Contraction of circular and longitudinal muscles, although phase-locked, do not appear to occur exactly synchronously in canine jejunum.

Animals↗
PubMedDate not supplied

Effect of the mycotoxins penitrem, paxilline and lolitrem B on the electromyographic activity of skeletal and gastrointestinal smooth muscle of sheep.

The electromyographic (EMG) activity of skeletal muscle was investigated as a method of recording the tremorgenic activity of the mycotoxins penitrem, paxilline and lolitrem B in sheep. EMG recordings were made concurrently from the abomasal antrum and duodenum to study the effects of these tremorgens on smooth muscle of the gut. Penitrem (2.2 to 7.5 micrograms kg-1) induced mild to moderate tremors within 15 to 20 minutes of injection which lasted for two to four hours. Paxilline (0.66 to 1.5 mg kg-1) induced mild to moderate tremors immediately which lasted for one to two hours. Lolitrem B (25 to 110 micrograms kg-1) had no effect at low doses, but at higher doses it produced tremors appearing over 20 to 30 minutes which persisted for more than 24 hours. The best measure of tremor indicated by skeletal muscle EMG was recorded from the shoulder area. The responses of smooth muscle of the antrum and duodenum to the tremorgens were variable. They included inhibitory effects on the antrum but no stimulation. The tremorgens had inhibitory effects on the duodenum on some occasions but on others, phase III migrating myoelectric complex-like activity was stimulated.

Acetone↗
PubMed1993

Gastrointestinal pacing.

Gastrointestinal pacing has been used to alter motor function and is effective in animal models in modulating gastric emptying, intestinal transit, and absorption. Application of gastrointestinal pacing to disorders of the human stomach and small bowel is an attractive treatment option that may some day become a clinical reality. Several technical problems must be overcome before further clinical testing can proceed.

Animals↗
PubMed1993

Normal physiology of small intestinal motility.

The small intestine produces a number of different contractions in various spatial and temporal patterns that promote efficient digestion, absorption, and propulsion of ingested material. The small bowel also serves a protective role through the use of special situation contractions that rapidly propel enteric contents into the stomach or colon, from which they may be expelled. Contractile activity of the small intestine is coordinated by an interplay of myogenic, neural, and chemical controls.

Animals↗
PubMed1993

Pathophysiology of small intestinal motility.

Only in the last few years have we begun to understand the effects of surgical procedures on contractile activity of the small intestine. Although most patients readily adapt to the procedures that are performed, operations such as small intestinal transplantation make it imperative that we pursue a more thorough understanding of the effects of surgery on the motility of the small intestine.

Animals↗
PubMed1993

Physiology of motor function of the sphincter of Oddi.

Human and experimental studies of the sphincter of Oddi have established that the sphincter is not a simple and passive smooth muscle portion of the biliary system; rather, it plays an active role in modulating bile flow into the duodenum in both the fasted and the postprandial states. The sphincter of Oddi in the opossum, and likely in man, demonstrates spontaneous phasic and perhaps peristaltic activity that affects bile flow into the duodenum. The sphincter appears to be under the control of a smooth muscle pacemaking-like region in the proximal sphincter that controls the frequency and direction of propagation of the phasic contractions. Immunohistochemical studies have documented the presence of dense concentrations of neuropeptide-containing myenteric nerves in the sphincter of Oddi. Physiologic studies have confirmed that these peptides, in combination with the classic gastrointestinal hormones, exert significant effects on biliary motility. Experimental studies of the motor physiology of the sphincter of Oddi have advanced our understanding of human biliary motility and dysmotility. A subset of patients experiences biliary-like pain after cholecystectomy. This pain may be attributable to either mechanical stenosis of the papilla or dysfunction of the sphincter of Oddi. No definitive test currently exists to establish the diagnosis with adequate sensitivity or specificity. It is hoped that further development of ultrasonographic, scintigraphic, manometric, or electromyographic techniques will allow a clearer definition of patients who truly have sphincter dysfunction and who might benefit from medical, endoscopic, or surgical therapy.

Animals↗
PubMed1996

Peripheral neurotensin participates in the modulation of pre- and postprandial intestinal motility in rats.

The present study was undertaken to determine whether neurotensin is involved in the regulation of the intestinal postprandial motor response and, if so, whether the regulatory pathway depends upon peripheral or central neurotensin secretion. Neurotensin, injected by the i.v. route (5 micrograms/kg) during the fasting state, induced firstly an increased irregular spiking activity during 30-40 min. This effect was followed by an increase of frequency of the myoelectrical complexes during 60 min. When injected by the i.c.v. route, neurotensin (0.5 microgram/kg) reinforced the fasting motility pattern of the small intestine after a latency of 70 min. Neurotensin was ineffective on the colon. The neurotensin receptor antagonist SR 48692 (200 micrograms/kg i.v.) reduced the duration of the postprandial motor response of the small intestine and blocked the late postprandial phase on the proximal colon while it suppressed the early postprandial phase on the distal colon. When administered i.c.v. (20 micrograms/kg), SR 48692 had no effect. It is concluded that neurotensin modulates intestinal postprandial motility essentially by a peripheral regulatory pathway. Endogenous neurotensin is involved in the maintenance of the postprandial motility pattern on the small intestine and the proximal colon while it is involved in the initiation of this response on the distal colon. This suggests that endogenous neurotensin acts via both endocrine and nervous mechanisms.

Animals↗
PubMed1998

Disinhibition during myoelectric complexes in the mouse colon.

Intracellular microelectrodes were used to record electrically evoked inhibitory junction potentials (IJPs) and electrotonic potentials during spontaneous cyclical depolarisations (myoelectric complexes, MCs) in the circular muscle layer of mouse colon in vitro. In the presence of nifedipine (1-2 microM) and atropine (1 microM), MCs were recorded every 264 +/- 18 s. Between MCs, single electrical stimuli (15 V, 0.6 ms, every 8 s) elicited IJPs whose amplitudes remained constant. In comparison, during the depolarising phase of MCs, the mean IJP amplitude was reduced by 61 +/- 7%, while during the late plateau and early repolarising phase of MCs, IJP amplitude was increased (up to 20%). NG-nitro-L-arginine (NOLA, 100 microM) abolished the repolarisation phase between MCs, so that the circular muscle remained depolarised and the amplitude of MCs was reduced by 73 +/- 6%. However, the amplitude of evoked IJPs was unaffected, as was the decrease in their amplitude during the depolarising phase of the residual MCs. In the presence of NOLA (100 microM), the further addition of apamin (250 nM) reduced the amplitude of evoked IJPs by approximately half. However, the amplitudes of NOLA- and apamin-resistant IJPs were also attenuated by 82 +/- 5% during the depolarising phase of residual MCs (amplitude: 1.9 +/- 1 mV). However, during this phase, the amplitude of an electrotonic potential (evoked by extracellular current application) was not attenuated. Addition of hexamethonium (500 microM), or tetrodotoxin (TTX) (1.6 microM) to solutions containing NOLA and apamin were without effect on membrane potential, but the residual MCs and the cyclical attenuation in IJP amplitude were abolished. During the intervals between MCs, membrane potential is maintained under tonic inhibition, via spontaneous release of inhibitory neurotransmitter(s), predominantly through nitrergic mechanisms. The cyclical attenuation in the amplitude of the non-nitrergic IJP does not arise from cyclical postjunctional changes in membrane resistance or potential. Moreover, the generation of the depolarising phase of MCs involves the simultaneous suppression of both nitrergic and non-nitrergic inhibitory neurotransmission. It is suggested that MCs arise from presynaptic suppression of ongoing inhibitory neurotransmitter release.

Animals↗
PubMed1998

Sympathetic pathways mediate GLP-1 actions in the gastrointestinal tract of the rat.

The aim of this study was to establish the actions of GLP-1 (7-37) on gastrointestinal motility in rats. We prepared anaesthetized Sprague-Dawley rats with strain-gauges in the antrum, duodenum and the proximal jejunum and a catheter in the aorta close to the coeliac artery for close infusion of substances. Intraarterial GLP-1 infusions (3 x 10(-10) and 3 x 10(-9) moles/kg per 10 min) (n = 8) induced inhibition of spontaneous motor activity in the antrum, duodenum and proximal jejunum. Inhibition induced by GLP-1 was reversed by i.v. infusion of GLP-1 receptor antagonist, Exendin (9-39) (3 x 10(-8) moles/kg per 10 min) (n = 6). Neither the presence of L-NNA (10(-5) moles/kg) (n = 9) nor the VIP receptor antagonist [4-Cl-D-Phe6, Leu17]-VIP (3 x 10(-8) moles/kg per 10 min) (n = 8) modified responses to GLP-1. However, a combination of the adrenergic blockers phentolamine and propranolol (1 mg/kg each) (n = 8) completely blocked motor actions of GLP-1 in all the organs studied. Moreover, inhibition of gastrointestinal motor activity by GLP-1 was blocked by previous infusion of hexamethonium (10 mg/kg) (n = 4). This study demonstrates that GLP-1 inhibits gastrointestinal motor activity of the rat acting on specific GLP-1 receptors and via stimulation of adrenergic pathways.

Animals↗
PubMed1998

Evidence that myoelectric complexes in the isolated mouse colon may not be of myogenic origin.

The hypothesis that spontaneous depolarisations (myoelectric complexes, MCs) can occur in the absence of neuronal activity, depending on the level of the membrane potential, was systematically studied. In control Krebs' solution, MCs were recorded approximately every 5 min and were abolished by tetrodotoxin (TTX, 1.6 microM). However, TTX also induced sustained membrane depolarisation (19 mV) in the circular muscle. To test whether MCs were blocked by the depolarisation induced by TTX, graded membrane repolarisations were generated, in the continuing presence of TTX, using sodium nitroprusside (SNP, 10 nM-1 microM). Under these conditions, MC activity was not restored. The addition of SNP (1 microM) to control preparations, in normal Krebs' solution, hyperpolarised the membrane of the circular muscle cells, but did not inhibit ongoing MC activity. It is suggested that the underlying mechanisms involved in MC generation are unlikely to be dependent upon the level of membrane potential in circular smooth muscle.

Animals↗