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PubMed1987

Gastrointestinal transit following intrathecal or subcutaneous narcotic analgesics.

This paper reports investigations on the effects on gastrointestinal transit of subcutaneous or intrathecal administration of opiates: morphine, sufentanil and alfentanil. Subcutaneous administration of opiates produced a significant dose-dependent decrease in transit of a charcoal meal test. Intrathecal administration of morphine to Wistar rats with catheter chronically implanted in the subarachnoid space did not cause a decrease in gastrointestinal transit. However, in freshly prepared rats with intrathecal catheter in the subarachnoid space, morphine significantly decreased intestinal transit of charcoal meal. In addition, sufentanil and alfentanil, on intrathecal administration in rats with chronically implanted catheters, caused a marked dose-dependent slowing of the passage of meal. Prior s.c. administration of the opiate antagonist naloxone completely blocked the depression of gastrointestinal transit caused by high doses of intrathecal sufentanil and s.c. administered morphine.

Alfentanil↗
PubMed1997

Contribution of gastrointestinal transit and pouch characteristics in determining pouch function.

AIM: To determine the contributions of gastrointestinal transit and pouch characteristics to bowel frequency in patients with an ileoanal reservoir and no pouchitis. METHODS: Twenty one patients who had undergone restorative proctocolectomy, with ileostomy closure at least eight months previously, and who had no history of pouchitis were recruited. They were prospectively classified on the basis of their bowel frequency: 11 patients had good pouch function (bowel frequency less than six per day) and 10 had poor function (bowel frequency more than six per day). Gastrointestinal transit was studied using a dual isotope technique and anal and pouch physiological examination was performed on all patients. RESULTS: Lag phase, 25% and 50% gastric emptying, small bowel transit time, and 10% and 50% pouch filling times, all for solids and liquids, were not significantly different between patients with good and poor function. Anal manometry and pouch and anal electrical sensitivity were also similar in the two groups. The volume of air and water required to elicit an initial sensation and the urge to defaecate were similar in both groups, but the maximum tolerated volume to both air (525 v 245 ml, good v poor function, median values) and water (625 v 370 ml) infusion was significantly (both p < 0.02) lower in patients with poor function. CONCLUSION: Maximum tolerated volume in the pouch, which may reflect pouch size, sensitivity, compliance, or a combination of these is the major determinant of pouch function. Gastrointestinal transit does not seem to be an important determinant of function.

Adult↗
PubMed2001

Slowing of gastrointestinal transit by oleic acid: a preliminary report of a novel, nutrient-based treatment in humans.

Chronic diarrhea may occur when gastrointestinal transit is abnormally rapid. We hypothesized that oleic acid given prior to a meal would slow gastrointestinal transit and reduce diarrhea by activating nutrient-triggered inhibitory feedback mechanisms in the small intestine. Transit time was measured in eight normal subjects following ingestion of a control emulsion (0 ml oleic acid), and in 45 patients with chronic diarrhea following ingestion of emulsions containing 0, 1.6, and 3.2 ml oleic acid. Stool volume and frequency on and off treatment were compared. Transit time in normal subjects was 102.4 +/- 11.2 min (mean +/- SE). Transit times in patients was shorter at 29.3 +/- 2.8 min with the 0-ml dose (P < 0.001), but increased to 57.2 +/- 4.5 min with the 1.6-ml dose and to 83.3 +/- 5.2 min with the 3.2-ml dose (P < 0.001). In the 18 patients who provided stool records, frequency of bowel movements decreased from 6.9 +/- 0.8 to 5.4 +/- 0.9 bowel movements/24 hr (P < 0.05) and stool volume decreased from 1829.0 +/- 368.6 to 1322.5 +/- 256.9 ml/24 hr with treatment (P < 0.05). An emulsion containing oleic acid slowed gastrointestinal transit and reduced diarrhea by activating nutrient-triggered inhibitory feedback mechanisms in the small intestine.

Adolescent↗
PubMed1983

Morphine tissue levels and reduction of gastrointestinal transit in rats. Correlation supports primary action site in the gut.

Overnight-fasted male rats given a single dose of tritium-labeled morphine either intraperitoneally or intravenously were fed a charcoal test meal by stomach tube. The drug remaining in tissues was assayed by liquid scintillation counting of thin-layer chromatograms from homogenates, and gastrointestinal transit was tested by measuring the portion of the small intestine traversed by charcoal in 5 min. Morphine, 0.15 mg/kg, given intraperitoneally either 10 min or 30 min before testing substantially reduced gastrointestinal transit (to 23% and 55% of drug-free controls, respectively), and produced maximum drug levels 5 min after administration in small intestine longitudinal muscle with attached myenteric plexus (500 +/- 42 ng/g, mean +/- SE, n = 4). Intact small intestine, plasma, and brain, respectively, contained decreasing drug concentrations that, in the latter, never exceeded 2%-3% of that in longitudinal muscle. Rats receiving 0.15 mg/kg morphine intravenously presented only minor and short-lived inhibition of gastrointestinal transit that was significantly below (approximately 35%) that of drug-free controls at 10 min, but not 30 min, after drug administration. Morphine levels in the brain and plasma of these rats were up to five times higher, and in the intact small intestine longitudinal muscle were up to 20 times lower than in intraperitoneally treated rats. Morphine concentration in the tissues assayed was plotted against the effect on gastrointestinal transit at the same interval for individual rats regardless of dose, administration route, and observation time: data analysis, in small intestine longitudinal muscle, but not in the brain or plasma, indicated a highly significant correlation and fitting of computer-generated curves described by a currently accepted equation according to the receptor occupation theory of drug response. In view of these findings, and of the complete prevention by the "peripherally selective" narcotic antagonist N-methyl naloxone of gastrointestinal transit inhibition after an intravenous analgesic dose of morphine (1 mg/kg), the investigated animal model is consistent with the primary role of a gut-located action site in opiate-induced constipation.

Animals↗
PubMed1993

Effect of saline cathartics on gastrointestinal transit time of activated charcoal.

The effects of saline cathartics on the gastrointestinal transit time of activated charcoal were investigated in six healthy volunteers. The study shows that the mean gastrointestinal transit times of charcoal alone were 29.3 h and 24.4, 15.4, 17.3 and 17.5 h with sodium chloride, sodium sulphate, magnesium sulphate alone and Andrew's Liver Salt respectively. Some volunteers complained of slight abdominal discomfort in all the phases except the Andrew's Liver Salt phase.

Adult↗
PubMed2000

Intestinal inflammation and morphine tolerance alter the interaction between morphine and clonidine on gastrointestinal transit in mice.

BACKGROUND: Morphine and clonidine show synergy or antagonism inhibiting gastrointestinal transit depending on their proportion and level of effect. Their interaction during morphine tolerance and intestinal inflammation were assessed. METHODS: Gastrointestinal transit in mice was evaluated with charcoal and antitransit effects expressed as percent mean values +/- SEM. Tolerance was induced with a morphine pellet (75 mg) implanted for 72 h, and inflammation with intragastric croton oil. Dose-response curves for morphine and clonidine alone and combined at a 1:1 potency ratio were obtained, and doses producing a 50% and 60% inhibition were calculated (ED50, ED60). Interaction was established by isobolograms, interaction indexes, and analysis of variance. RESULTS: In naive and tolerant mice, the combination induced linear dose-response curves up to the ED60 and then reached a plateau. In naive mice, ED50 values were as follows: morphine 1.52 +/- 0.15 mg/kg, clonidine 0.09 +/- 0.008 mg/kg, and combined 0.506 +/- 0.084 mg/kg (0.478 +/- 0.08 mg/kg morphine plus 0.028 +/- 0.004 mg/kg clonidine). During tolerance, ED50 values were as follows: morphine 9.73 +/- 0.8 mg/kg, clonidine 0.09 +/- 0.007 mg/kg, combination 0.131 +/- 0.09 mg/kg (morphine 0. 13 +/- 0.09 mg/kg plus clonidine 0.0013 +/- 0.0005 mg/kg). In both groups, the interaction was synergistic up to the ED60 and antagonistic thereafter; synergy was enhanced during tolerance. During inflammation, ED50 values were as follows: morphine 0.17 +/- 0.04 mg/kg, clonidine 0.015 +/- 0.006 mg/kg, combined 0.62 +/- 0.04 mg/kg (morphine 0.568 +/- 0.04 mg/kg plus clonidine 0.052 +/- 0.004 mg/kg); thus, potencies of morphine and clonidine increased 9.3 and 7.1 times, while the combination remained unaltered. Moreover, inflammation transformed synergy into antagonism. CONCLUSIONS: The interaction between morphine and clonidine was significantly altered during tolerance and inflammation. During tolerance, synergy was present up to 60% effect and then became antagonistic. Inflammation converted synergy to antagonism. A common pathway in signal transduction could partially explain the results.

Analgesics↗
PubMed1988

Effect of substance P on rat gastrointestinal transit.

The in vivo effect of substance P and related peptide analogs on gastrointestinal transit in unanesthetized rats was studied. Fasted male rats were given intragastrically 0.5 ml of a powdered charcoal (BaSo4.H2O) meal and were concomitantly injected intraperitoneally with 8 micrograms/kg of substance P or a related peptide. In control rats, the percentage of small intestine traversed by the meal 15 min after feeding was 44.9 +/- 1.4 (N = 12). Substance P, [pGlu6]SP, [pGlu6, gPhe8, mGly9]SP and [pGlu5, N-MePhe8, N-MeGly9]SP significantly accelerated intestinal transit: 59.5 +/- 3.1% (N = 7); 66.0 +/- 3.8% (N = 14), 66.8 +/- 2.4% (N = 25), and 58.4 +/- 4.4% (N = 4), respectively. Concomitant injection of [pGlu6]SP and BOC-Phe-Phe-Gly-NHOH, an inhibitor of enzyme degradation at a dose of 800 micrograms/kg lowered by 10-fold the dose of [pGlu6]SP needed to induce the same degree of intestinal transit acceleration. These results indicate that in rats, substance P and related peptides accelerate gastrointestinal transit.

Animals↗
PubMed1995

A new pharmacokinetic model including in vivo dissolution and gastrointestinal transit parameters.

When dissolution is the rate-limiting step in absorption of a drug, both it and gastrointestinal transit can play dominant roles in determining absorption. Therefore, a pharmacokinetic model including the process of dissolution, gastrointestinal transit rate and gastrointestinal pH profile was proposed to explain the behavior of drug formulations in vivo. Clarithromycin (CAM), which exhibits pH-dependent solubility and has high partition coefficients, was used as a drug to test the model, and the effect of a meal on serum concentrations of CAM after a single oral administration to healthy volunteers was evaluated. The results of pharmacokinetic analyses of serum concentration-time data for a single oral administration of CAM to humans in the fasting and postprandial states were well fitted by the new pharmacokinetic model. By substituting the pharmacokinetic parameters obtained into the model equations, the in vivo rate of dissolution could be determined. Pharmacokinetic parameters affecting drug bioavailability were also examined using the model. Factors influencing the behavior of a drug formulation in the gastrointestinal tract were determined. These findings indicate that the model we have proposed can be used to evaluate the behavior of drug formulations in vivo.

Clarithromycin↗
PubMed1985

Gastrointestinal transit time in human pregnancy: prolongation in the second and third trimesters followed by postpartum normalization.

Fifty-nine studies of gastrointestinal transit time were performed in 27 healthy women during pregnancy and postpartum. Gastrointestinal transit time was defined as the time of the first sustained rise in breath hydrogen concentration after ingestion of 10 g of lactulose. Gastrointestinal transit time was significantly prolonged in both the second and third trimesters of pregnancy (125 +/- 48 min and 137 +/- 58 min, respectively) when compared with either the first trimester of pregnancy or the postpartum period (99 +/- 39 min and 75 +/- 33 min, respectively). Transit times measured in the first trimester were not significantly different from those postpartum. Because the prolongation of transit time in late pregnancy is transient, it is probably due to hormones (perhaps progesterone) or other metabolic effects of pregnancy.

Adolescent↗
PubMed1994

Gastrointestinal transit through esophagus, stomach, small and large intestine in patients with progressive systemic sclerosis.

Liquid esophageal transit and gastric emptying, mouth-to-cecum transit, and whole gut transit of a solid-liquid meal were measured in 14 patients with PSS, 16 control subjects (esophageal transit), and 20 control subjects (gastrointestinal transit), respectively, by using scintigraphic techniques, the hydrogen breath test, and stool markers. In patients with PSS, the glucose hydrogen breath test for detection of small intestinal overgrowth was performed and various gastrointestinal symptoms were determined. Esophageal transit and gastric emptying were significantly prolonged in PSS patients with 11 of 14 PSS patients (79%) disclosing delayed esophageal transit and eight of 14 PSS patients (57%) disclosing delayed gastric emptying. All PSS patients with prolonged gastric emptying also had delayed esophageal transit and there was a significant positive correlation between esophageal transit and gastric emptying (r = 0.696, P < 0.01). No significant differences between PSS patients and controls were detected concerning mouth-to-cecum transit and whole gut transit, but abnormally delayed mouth-to-cecum transit was found in four of 10 PSS patients (40%) and abnormally prolonged whole gut transit was detected in three of 13 PSS patients (23%). Small bacterial overgrowth was diagnosed in three of 14 PSS patients (21%). Delayed esophageal transit and gastric emptying were associated with dysphagia, retrosternal pain, and epigastric fullness, while prolonged whole gut transit was associated with constipation. It is concluded that delayed gastric emptying is frequently associated with esophageal transit disorders in PSS patients and may be one important factor for the development of gastroesophageal reflux disease in these patients.

Adult↗
PubMed1995

Hyperglycaemia is responsible for the inhibited gastrointestinal transit in the early diabetic rat.

The effect of plasma glucose levels on the gastrointestinal motility of the rat was studied. Chronic hyperglycaemia was induced by i.v. injection of streptozotocin 1 week before the motility experiment. Some rats received additional daily insulin therapy (1.25, 2.5 or 10 IU kg-1) after induction of diabetes mellitus. Acute hyperglycaemia was induced by the continuous i.v. infusion of glucose solution (11, 22, 44 or 88 mg kg-1 min-1) 10 min before the motility experiments. The rats were killed 15 min after successful orogastric feeding of a charcoal-contained suspension. Gastrointestinal transit was calculated as the percentage of the overall length of the small intestine to which the charcoal moved during this time period. The diabetic rats were found to have delayed transit compared with controls (mean +/- SEM: 32.2 +/- 2.1% vs. 42.9 +/- 4.2%, P < 0.05). Correction of hyperglycaemia with moderate doses of insulin therapy failed to inhibit transit, whereas hypoglycaemia induced by high-dose insulin treatment enhanced transit. High doses of glucose elicited acute hyperglycaemia and delayed transit when compared with saline infused non-diabetic rats. In early diabetes, hyperglycaemia probably mediates the inhibited gastrointestinal transit, since correction of hyperglycaemia usually restores the delayed transit.

Acute Disease↗
PubMed1986

Intrathecal bombesin-induced inhibition of gastrointestinal transit: requirement for an intact pituitary-adrenal axis.

The role of the pituitary-adrenal axis in the inhibition of gastrointestinal transit caused by intrathecal administration of bombesin was examined. Bombesin (0.3-10 micrograms) slowed transit by this route in a dose-related manner. Either hypophysectomy or adrenalectomy prevented the inhibition of gastrointestinal transit associated with bombesin (10 micrograms, i.th.). The inhibitory gut effects of this peptide were not prevented in sham-operated rats. Intrathecal bombesin-induced inhibition of gastrointestinal transit is thus dependent upon an intact pituitary-adrenal axis.

Adrenal Glands↗
PubMed1990

Role of peripheral mu, delta and kappa opioid receptors in opioid-induced inhibition of gastrointestinal transit in rats.

The roles of various types of opioid receptors in opioid-induced local inhibition of gastrointestinal transit were studied in rats 5 min after a charcoal meal, injecting i.p. relatively selective agonists and antagonists. The proposed mu agonists, morphine and [D-Ala2,MePhe4,Gly-ol5]enkephalin (DAMGO), and the nonselective delta agonist, [D-Ala2,D-Leu5]enkephalin (DADLE), produced a dose-related inhibition of gastrointestinal transit at the peak time and the i.p. doses producing a 50% reduction of the control values (A50) were 0.015, 0.006 and 0.023 mg/kg, respectively, for morphine, DAMGO and DADLE. The effect of the other nonselective delta agonist, [D-Ser2,L-Leu5]enkephalyl-Thr (DSLET), was not linearly related with the dose. The proposed selective delta agonist, [D-Pen2,D-Pen5]enkephalin (DPDPE), and the selective kappa agonist, U-69,593, up to 2 and 15 mg/kg i.p., respectively, did not delay gastrointestinal transit. Naloxone (0.05 mg/kg i.p.) injected 1 min before each agonist produced a significant parallel shift to the right of the dose-response curves for morphine and DAMGO, but only partly antagonized the effects of DADLE and DSLET. The selective delta antagonist ICI 174,864 (1 mg/kg i.p., injected 1 min before each agonist) shifted the dose-response curve of DADLE, but not of the mu agonists, slightly, but significantly to the right, and had an inconsistent effect on DSLET. Naloxone prevented DADLE's effect on the gut with a nonlinear dose-response curve and much higher doses of naloxone were required to prevent fully DADLE-induced effects than to antagonize doses of morphine equiactive to DADLE on the gut.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Development of tolerance to the inhibitory effect of loperamide on gastrointestinal transit in mice.

The inhibitory effect of repetitiously administered loperamide, a peripheral mu-opioid receptor agonist and well-recognized antidiarrheal agent, on mouse gastrointestinal transit was compared with that of morphine in order to examine the development of tolerance to mu-opioid receptor agonist-induced constipation (antitransit effect). When administered subcutaneously 15 min before the oral injection of charcoal meal, loperamide (0.1-30 mg/kg) and morphine (1-8 mg/kg) dose-dependently and significantly inhibited gastrointestinal transit of charcoal with the ID(50) values of 1.6 (0.3-7.1) mg/kg and 3.6 (1.5-8.5) mg/kg, respectively. When loperamide (30 mg/kg) was administered twice daily for 2 days, the antitransit effect was significantly reduced. On the other hand, morphine did not develop tolerance in even more severe conditions than those of loperamide. It is known that P-glycoprotein, an ATP-dependent drug efflux pump, is involved in the development of tolerance to morphine analgesia. The tolerance observed with loperamide was significantly prevented by cyclosporin (30 mg/kg, i.p.), a P-glycoprotein inhibitor, thus the ID(50) value in loperamide-tolerant mice was markedly reduced from >1000 mg/kg to 40 (2.7-603.0) mg/kg by cyclosporin. These results indicate that loperamide, different from morphine, readily develops tolerance to the inhibitory effect on mouse gastrointestinal transit, and the P-glycoprotein may be involved in the development of tolerance to the antitransit effect of loperamide.

Animals↗
PubMed1985

Effect of selective and non-selective antimuscarinics on rectosigmoid motility and gastrointestinal transit.

In 12 healthy volunteers, a rectosigmoid motility index (RSMI) was measured when either placebo, 0.5 mg atropine, or 5 mg pirenzepine was given intravenously as a single dose, double-blind, in random order after a control period of 30 min. Compared with the control period, atropine gave a significant decrease of the RSMI during the entire recorded period of 90 min, whereas pirenzepine inhibited RSMI only during the first two 15-min periods. In another series of experiments, gastrointestinal transit was assessed by means of a radiographic marker method. In healthy volunteers, gastrointestinal transit was estimated (n = 20) and gastric secretion was measured (basally and after modified sham feeding; n = 10) during oral medication with placebo, 50 mg pirenzepine twice daily, or 17.5 mg benzilonium bromide twice daily. In 10 of the volunteers gastrointestinal transit was also estimated with 35 mg benzilonium bromide twice daily, and in the other 10 volunteers with 0.6 mg L-hyoscyamine twice daily. The number of retained markers was significantly lower during pirenzepine than during L-hyoscyamine treatment. Neither dose of benzilonium bromide changed the transit of markers. Compared with non-selective antimuscarinics, the effect of pirenzepine was differential: with equipotently acid-reducing doses the decrease of the RSMI after pirenzepine lasted shorter and gastrointestinal transit was accelerated.

Adult↗
PubMed1986

Independent central and peripheral mediation of morphine-induced inhibition of gastrointestinal transit in rats.

The individual contributions of central (brain) and peripheral (enteric) sites in the mediation of the systemic actions of opioids are not well established. In this study, we made use of naltrexone methobromide, a quaternary analog of naltrexone, to separate the central and peripheral components of the slowing action of morphine on gastrointestinal transit in rats. It was established that i.c.v., but not s.c., administration of quaternary naltrexone antagonized morphine-induced analgesia in the radiant-heat tail-flick assay in rats. Thus, quaternary naltrexone probably does not enter the central nervous system in significant amounts after systemic administration. Systemic quaternary naltrexone antagonized, in a dose-related manner, the delaying effects of morphine on the movement of a charcoal meal along the gastrointestinal tract. Quaternary naltrexone was 30 or 100 times less potent than naltrexone when administered s.c. or i.c.v., respectively. Unlike naltrexone, quaternary naltrexone antagonized morphine-induced slowing of gastrointestinal transit only when administered by the same route (i.e., both s.c. or both i.c.v.). The apparent pA2 for s.c. quaternary naltrexone against s.c. morphine was not significantly different from the apparent pA2 for i.c.v. quaternary naltrexone against i.c.v. morphine. Distinct and independent central and peripheral systems appear to mediate morphine-induced inhibition of gastrointestinal transit in rats. However, the receptors are probably of the same type. Peripherally selective antagonists such as quaternary naltrexone may be useful in reversing morphine-induced inhibition of gastrointestinal transit without affecting analgesia.

Analgesia↗
PubMed2005

Excipient effects on gastrointestinal transit and drug absorption in beagle dogs.

Previous work has shown that polyethylene glycol 400 (PEG 400) has an accelerating effect on gastrointestinal transit and a modulating influence on drug absorption in humans. The aim of this study was to assess the impact of various excipients, PEG 400, propylene glycol, d-alpha-tocopheryl-polyethylene glycol-1000 succinate (TPGS) and Labrasol on gastrointestinal transit and drug absorption in four beagle dogs using scintigraphy. Each dog received, on five separate occasions, water (control) or a dose of excipient equivalent to 1 g PEG 400, 2 g propylene glycol, 1 g TPGS or 2 g Labrasol dissolved in water and administered in the form of two capsules. The model drugs ampicillin (200mg) and antipyrine (100mg) were co-administered in the capsules. The capsule solutions were radiolabelled with technetium-99m to follow their transit using a dual-headed gamma camera, and blood samples were collected to determine drug pharmacokinetics. On a separate occasion, the drugs were dissolved in saline and given intravenously. The capsules rapidly disintegrated in the stomach liberating their liquid contents. The mean small intestinal transit times for the different treatments (control, PEG 400, propylene glycol, TPGS and Labarasol) were 183, 179, 195, 168 and 154 min, respectively. The corresponding mean absolute oral bioavailability figures were 36, 32, 39, 42 and 32% for ampicillin and 76, 74, 85, 73 and 74% for antipyrine, respectively. The transit and bioavailability data for the excipient treatments were not significantly different from the control. In summary, these excipients, at the doses administered, have limited influence on gastrointestinal transit and drug in beagle dogs.

Ampicillin↗
PubMed2000

Functional magnetic stimulation facilitates gastrointestinal transit of liquids in rats.

The purpose of this study was to investigate the effect of a relatively novel technology, functional magnetic stimulation (FMS), on gastrointestinal transit of liquids in rats. Orogastric gavage with technetium-99 solution was used to assess gastric emptying and gastrointestinal transit time in 92 rats. FMS was performed over the anterior cervical and/or dorsal thoracolumbar regions using a figure-8 coil. Stimulation protocols were 1, 2, or 4 h in length. FMS accelerated gastric emptying and decreased gastrointestinal transit time. The acceleration was dependent on the stimulation parameters used as well as on the duration of the protocol; high levels of FMS produced a quicker effect, whereas lower levels were effective at later times. This study provides evidence that FMS could be an alternative or adjunct therapy to treat disorders in gastrointestinal motility.

Analysis of Variance↗