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Results for “GASTROINTESTINAL MOTILITY”

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At least 19 recordsLinked to original sources
PubMed1989

Postoperative pain relief and gastrointestinal motility.

Gastrointestinal motility is normally inhibited for 2-3 days after abdominal surgery. The methods used for postoperative pain relief may themselves also influence gastrointestinal function. Although parenteral and epidural administration of opioids delays gastric emptying and prolongs intestinal transit time, epidural anesthesia with local anesthetics does not influence gastrointestinal motility in volunteers. Clinical studies show that epidural anesthesia does not delay gastric emptying or prolong intestinal transit time as much as parenteral and epidural opioids. Therefore, for postoperative pain relief after abdominal surgery, epidural anesthesia with local anesthetics seems the best alternative to avoid or minimize adverse effects on gastric emptying and intestinal motility.

Anesthesia, Epidural↗
PubMed1993

[Experimental gastrointestinal motility].

Gastrointestinal motility is a major field of research today; however, despite there being a huge amount of available data in the literature, its exact role as a diagnostic tool has yet to be defined. The purpose of this paper is to describe some of the existing experimental models and methods for conducting motility studies.

Animals↗
PubMed1987

The in vivo effect of ethanol on gastrointestinal motility and gastrointestinal handling of calcium in rats.

The acute effects of an intragastric administration of ethanol (2 g/kg body weight) (given as 13.3% w/v solution) on the in vivo gastrointestinal motility and gastrointestinal absorption and secretion of calcium were investigated in 20-h fasted rats. Gastric ethanol concentration remained high for 90 min while the concentration in the duodenum peaked at 30 min before declining to a range slightly higher than that in the mid- and distal intestine. Plasma ethanol peaked at 60 min. From the polyethylene glycol (PEG) distribution, ethanol was found to delay gastric emptying, and at 60 min, 40% of PEG was still retained in the stomach of the ethanol-treated group while gastric emptying had been completed in the controls. However, ethanol placed directly into the duodenum was found to enhance intestinal motility. Under control conditions, exogenous calcium was completely absorbed by the time it reached the mid-small intestine (J3) and calcium found in more distal segments was of endogenous origin. Ethanol suppressed calcium absorption while markedly stimulating calcium secretion in the stomach and the distal small intestine, resulting in a net 32% increase in the total gastrointestinal calcium content. This effect on the distal small intestine was from ethanol that had reached this area from the circulation, and not from ethanol transit along the gastrointestinal tract.

Animals↗
PubMed2003

Gastrointestinal motility disorders and gastrointestinal prokinetic therapy.

Gastrointestinal motility disorders represent a diagnostic and therapeutic challenge. Disorders of gastrointestinal motility may result in accelerated transit, delayed transit, impaired relaxation, or inappropriate relaxation. The delayed transit disorders are the most important motility disorders of companion animals and may involve the esophagus (hypomotility and megaesophagus), stomach (delayed gastric emptying), small intestine (postoperative ileus and intestinal pseudo-obstruction), or colon (constipation and megacolon).

Animals↗
PubMed1990

Effects of a new 1,4-dihydropyridine, lacidipine, on gastrointestinal motility and other gastrointestinal functions.

Lacidipine is a new 1,4-dihydropyridine calcium entry blocker endowed with slow onset of action and potent and long-lasting antihypertensive activity. This study investigated the effect of lacidipine on some gastrointestinal functions, mainly gastrointestinal motility, in rats and dogs. In fasting conscious dogs chronically fitted with electrodes and strain gauges along the small bowel, lacidipine (12 micrograms/kg i.v. bolus or 10 micrograms/kg/h for 3 h) did not modify the migrating motor complex pattern or intestinal spike activity. In the rat, lacidipine proved less active (ED 50 greater than 100 mg/kg p.o.) than nitrendipine (ED 50 = 31 mg/kg p.o.) in inhibiting gastric emptying of a liquid meal, whereas the opposite was true after a solid meal (ED 50 = 10.9 and 35.0 mg/kg p.o., respectively). Lacidipine inhibited fecal pellet output at lower doses (ED 50 = 14.8 mg/kg p.o.) than nitrendipine (ED 50 = 40.1 mg/kg p.o.). On histamine-induced gastric acid secretion, the effect of 100 micrograms/kg i.v. lacidipine was moderate (maximum inhibition 45%). The gastrointestinal effects displayed by lacidipine appear at doses at least 5 and 50 times as high as those affecting blood pressure after intravenous and oral administration, respectively. Thus, lacidipine is unlikely to cause noteworthy unwanted effects on the gastrointestinal tract.

Animals↗
PubMed2001

The use of endoscopy in patients with gastrointestinal motility problems.

Gastrointestinal motility disorders are a commonly encountered problem. Although some are associated with organic alterations, others are defined by their symptoms, and no anatomic or histologic organic changes are to be found. In most cases, the etiology is completely unclear. Endoscopy, with the option of obtaining biopsies for histopathologic evaluation, plays the most important role in the diagnostic workup, as it can exclude such lesions as tumors, ulcers, inflammatory processes, and diverticula and it helps to define the grade and extent of motility-associated diseases (e.g., GERD). Furthermore, endoscopic interventional procedures offer sufficient treatment of several motility-related disorders (e.g., achalasia, GERD, its associated diseases, secondary constipation).

Colonic Diseases, Functional↗
PubMed1995

Gastrointestinal motility in obesity.

Gastrointestinal motility is closely linked to the rate at which nutrients become systemically available. Regulation of gastric emptying represents the most important brake against delivery of nutrients to the intestine in excess of digestive and absorptive capacity. In man, gastric emptying is slowed in proportion to the energy density of the meal, which will level out the rate of energy delivery to the duodenum. Studies suggest a more rapid gastric emptying in obesity, although the opposite has been reported in some experimental settings. Moreover, gastric volume is larger in obese individuals and appropriate satiety signals are not triggered in response to gastric distension. Postprandial intestinal transit time in obesity is similar to that in normal-weight subjects, however, despite this fact, intestinal absorption of nutrients is more efficient in obesity. Several regulatory mechanisms for gastrointestinal motility, such as the autonomous and enteric nervous systems and gastrointestinal regulatory peptides, are also of importance for feeding behaviour and metabolism. Dysfunction of the autonomous nervous system has been observed, the sensitivity to cholecystokinin is decreased in obesity, and plasma concentrations of somatostatin and neurotensin are lower than in normal-weight subjects. These changes in regulatory mechanisms favour rapid gastrointestinal transit of ingested nutrients and promote rapid intestinal absorption in obesity and decreased satiety in response to ingested food. It is presently not known whether the observed changes in gastrointestinal motility in obesity represent a primary feature linked to the pathogenesis of such disease.

Autonomic Nervous System↗
PubMed1991

Role of fasting gastrointestinal motility in the variability of gastrointestinal transit time assessed by hydrogen breath test.

Gastrointestinal motility and transit time, measured by the hydrogen breath test, were simultaneously assessed in six healthy volunteers. Each subject underwent six studies on separate days. On each day motility was measured in the gastric antrum, duodenum, and proximal jejunum and 15 g of lactulose was given either by mouth during gastric phases I, II, III of the motor migrating complex or infused duodenally during duodenal phases I, II, III, one phase being studied each day in random order. Fasting activity was not interrupted by the lactulose. The lactulose transit time decreased significantly from a peak with phase I through phase II to a minimum with phase III (mean (SD) 155 (26) min v 120 (10) min v 94 (14) min, p less than 0.001). Similar results were noted when the lactulose was instilled intraduodenally (156 (23) min v 125 (19) min v 100 (17) min, p less than 0.001). No correlation was found between motility index and transit. These results suggest that different phases of fasting gastrointestinal motility are major determinants of the transit time estimated by the hydrogen breath test and explain the variability of this test in practice.

Administration, Oral↗
PubMed1977

Extrinsic neural influences on gastrointestinal motility.

The gastrointestinal tract is capable of carrying on all its major functions after all extrinsic nerves have been cut. This automaticity is due to the local nervous mechanisms in the walls of the gastrointestinal tract and the inherent properties of the smooth muscles in its walls, and gastrointestinal hormones. All levels of the central nervous system have been shown, by stimulation and ablation studies, to influence the motility of the entire gastrointestinal tract. Throughout many cerebral areas there are loci which, on stimulation, exert both inhibitory, and less often, excitatory influence on gastrointestinal motility. These influences are mediated by sympathetic and parasympathetic visceral efferent nerves, as well as humoral agents from the neurohypophysis. Thus, they impose an influence of higher control on the automatically efficient intrinsic motility. They are guided by information received from visceral, cranial, and somatic afferents, as well as intracerebral, or psychic inputs. Under normal circumstances they only influence gastrointestinal activity as will best afford the optimal functioning of a performance done automatically with efficiency and finesse.

Afferent Pathways↗
PubMed1991

[Central regulation of gastrointestinal motility and secretion].

Gastrointestinal motility and secretions are regulated by cerebral nuclei via autonomic efferents in a coordinated fashion. At rest, vagal activity dominates while during different forms of stress the activated sympathetic nervous system markedly modulates secretions and motility. Expression of unique neuropeptides in distinct CNS regions facilitates the differentiated regulation of visceral functions. For example, corticotropin-releasing factor regulates the homeostatic pattern of visceral functions during stress. Furthermore, thyrotropin-releasing hormone accounts for parasympathetic activity while calcitonin gene related peptide predominantly accounts for sympathetic modulation of gastrointestinal motility and secretions. These neuropeptides coordinate visceral functions producing integrated motor and secretory responses that facilitate diverse digestive processes.

Animals↗