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Results for “Gastrointestinal Transit”

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At least 19 recordsLinked to original sources
PubMed2003

Etiology of portal hypertension may influence gastrointestinal transit.

BACKGROUND: Gastrointestinal transit studies have shown contradictory results in patients with portal hypertension. We have studied gastric emptying. small-bowel transit and colonic transit in patients with portal hypertension. The association between small-bowel bacterial overgrowth and gastrointestinal transit was assessed. METHODS: Sixteen patients (6 females) with portal hypertension and esophageal varices were included. A newly developed radiological procedure was used to measure gastrointestinal transit during one visit. Variceal pressure was measured and culture of small-bowel aspirate was used to diagnose small-bowel bacterial overgrowth. The results were compared to results obtained in 83 healthy subjects. RESULTS: Half gastric emptying time in male patients was 3.8 (0.9-5.8) h versus 2.5 (0.4-4.0) h in healthy males (median and percentile 10-90: P < 0.05). Small-bowel residence time in male patients was 5.9 (2.0-13.7) h versus 3.2 (1.5-6.0) h in healthy males (P < 0.05). Small-bowel residence time in patients with bacterial overgrowth was significantly longer than in patients without bacterial overgrowth. Small-bowel residence time was also significantly longer in male patients with alcoholic cirrhosis as compared to male patients with other causes of portal hypertension. Colonic transit in all patients and gastric emptying and small-bowel transit in female patients were not significantly different from healthy subjects. CONCLUSION: Etiology of liver disease and gender may influence transit in patients with portal hypertension. Small-bowel bacterial overgrowth was associated with delayed small-bowel transit.

Adolescent↗
PubMed2005

A new tactic to treat postprandial hyperlipidemia in diabetic rats with gastroparesis by improving gastrointestinal transit.

Improvement of gastrointestinal transit was thought to be a new tactic to treat postprandial hypertriglyceridemia in diabetic individuals with gastroparesis. Diabetic gastroparesis, lipid load testing, and the effect of domperidone or aqueous extract of rhizomes of Rheum palmatum L. on postprandial hypertriglyceridemia were evaluated in alloxan-induced diabetic rats. Alloxan diabetic animals had a slow gastrointestinal transit, together with delayed and exaggerated postprandial hypertriglyceridemia, after oral administration of olive oil, which was significantly improved after oral administration of domperidone or R. palmatum L. However, atropine could prevent the effects of R. palmatum L. The reduced postprandial hypertriglyceridemia was highly correlated with the improvement in gastrointestinal transit. These results suggest that promotion of gastrointestinal transit may be useful for the treatment of postprandial hypertriglyceridemia in diabetic patients with gastroparesis. R. palmatum L. may become a new choice for these patients since it has more potential benefits than domperidone.

Administration, Oral↗
PubMed2006

Ghrelin improves burn-induced delayed gastrointestinal transit in rats.

Delayed gastrointestinal transit is common in patients with severe burn. Ghrelin is a potent prokinetic peptide. We aimed at testing the effect of ghrelin on burn-induced delayed gastrointestinal transit in rats. Gastric emptying (GE), intestinal transit (IT), and colonic transit (CT) studies were performed in male Sprague-Dawley rats. Rats were randomized into two main groups as follows: sham injury and ghrelin-treated burn injury with doses of 0, 2, 5, and 10 nmol/rat ip 6 h after burn. Sham/burn injury was induced under anesthesia. Rats received a phenol red meal 20 min following ghrelin injection. Based on the most effective ghrelin dose, 1 mg/kg sc atropine was given 30 min before the ghrelin in one group of rats for each study. The rats in each group were killed 30-90 min later; their stomachs, intestines, and colons were harvested immediately, and the amount of phenol red recovered was measured. Percentage of gastric emptying (GE%) and geometric center for IT and CT were calculated. We found 1) severe cutaneous burn injury significantly delayed GE, IT, and CT compared with sham injury (P < 0.05); 2) ghrelin normalized both GE and IT, but not the CT; 3) the most effective dose of ghrelin was 2 nmol/rat; and 4) atropine blocked the prokinetic effects of ghrelin on GE% and IT. In conclusion, ghrelin normalizes burn-induced delayed GE and IT but has no effect on CT in rats. The prokinetic effects of ghrelin are exerted via the cholinergic pathway. Ghrelin may have a therapeutic potential for burn patients with delayed upper gastrointestinal transit.

Animals↗
PubMed1987

The effect of nalbuphine on gastrointestinal transit in mice.

Nalbuphine given subcutaneously (s.c.) inhibited gastrointestinal transit in a dose-dependent manner. Prior s.c. administration of naloxone hydrochloride suppressed the inhibitory effect of nalbuphine on gastrointestinal transit. Naloxone methobromide (naloxone MB), a quaternary compound, was also effective in antagonising this effect of nalbuphine but was less effective than naloxone hydrochloride. Furthermore, prior s.c. administration of Mr 2266 also antagonised the gastrointestinal transit inhibitory action of nalbuphine. When given centrally, either intracerebroventricularly (i.c.v.) or intracisternally (i.c.), naloxone hydrochloride was ineffective in antagonising s.c. nalbuphine. Similar findings were observed with centrally administered Mr 2266. In addition, i.c. nalbuphine had a minimal effect on gastrointestinal transit while i.c.v. nalbuphine only caused slight inhibition of gastrointestinal transit. It was concluded that nalbuphine inhibits gastrointestinal transit mainly through peripheral opiate receptors.

Animals↗
PubMed1997

Prediction of the plasma concentration profiles of orally administered drugs in rats on the basis of gastrointestinal transit kinetics and absorbability.

A new method based on gastrointestinal transit kinetics has been developed for estimation of the absorption profiles of drugs administered orally as aqueous solutions. The utility of the method was evaluated in rats. The gastrointestinal transit profile for each segment was estimated by in-vivo studies using phenol red, an unabsorbable marker. The gastrointestinal transit profile of phenol red was well explained by a linear gastrointestinal transit kinetic model with eight segments. We also introduced the absorption process into the gastrointestinal transit kinetic model and the plasma profile was predicted by the convolution method. The absorbability of drugs in each segment was assessed by an in-situ absorption study. The validity of the model was evaluated for model drugs with different absorption characteristics. The plasma profiles predicted for ampicillin, theophylline and cephalexin were in good agreement with those observed. The overestimated plasma profile of propranolol suggests that the low bioavailability of propranolol is a result of first-pass metabolism by the intestine wall and the liver, because the calculated absolute absorption is almost perfect. This proposed model is also suitable for estimation of segmental absorption, which is useful for the development of drug delivery systems. We have demonstrated that the plasma profile of orally administered drugs can be predicted by use of gastrointestinal transit and segmental absorbability information and that this method is especially useful for estimating separately the effect of absolute absorption and first-pass metabolism on the bioavailability of drugs.

Administration, Oral↗
PubMed1988

Comparison of the effects of psyllium and wheat bran on gastrointestinal transit time and stool characteristics.

Gastrointestinal transit time, frequency of defecation, stool weight, and stool consistency were studied in 12 subjects who were each given fiber supplements containing wheat bran, psyllium gum, a combination of wheat bran and psyllium gum, or a low-fiber control for 2 weeks. Gastrointestinal transit time was measured using four different markers: plastic pellets, chromium mordanted bran, cobalt-ethylenediamine-tetraacetic acid, and terbium oxide. The wet weight and dry weight of stools were measured, and a questionnaire accessed subjects' perceptions of the consistency of their stools. Fiber supplementation decreased transit time and increased the daily number of defecations and the wet weight and dry weight of stools. Bran had a greater effect on transit time than psyllium. Psyllium had a greater effect on the amount of water found in the stools and the total stool weight. On the days that stools were passed, 50% of the daily stool ratings were scored as "hard" when subjects received the control supplement. Less than 10% of the ratings were scored as "hard" when subjects received the high-fiber supplements. The type of marker used did not significantly affect the transit time measured.

Adult↗
PubMed1981

Gastrointestinal transit: the effect of the menstrual cycle.

Gastrointestinal transit time as well as serum estradiol and progesterone levels were measured in 15 normally menstruating women twice during their menstrual cycle, once in the follicular phase (days 8-10) when progesterone levels are low and once in the luteal phase (days 18-20) when progesterone levels are increased. Each subject had a progesterone rise during the luteal phase and onset of menses at the expected time documenting ovulatory cycles. Gastrointestinal transit time from ingestion of lactulose to the delivery of the disaccharide to the cecum was determined by monitoring breath hydrogen levels at 10-min intervals. Gastrointestinal transit time was significantly (p less than 0.01) prolonged in the luteal phase when progesterone levels were increased compared with the follicular phase. This study demonstrates that the menstrual cycle plays an important role in determining the gastrointestinal transit time in normally menstruating women.

Adult↗
PubMed2001

Biphasic alterations in gastrointestinal transit following endotoxaemia in mice.

Lipopolysaccharide (LPS)-induced alterations of gastrointestinal transit were studied in mice using activated charcoal. LPS (10 mg kg-1) induced biphasic alterations of intestinal transit. Increase (acceleration phase) and delay (lag phase) in gastrointestinal transit were observed at 90 and 480 min after LPS injection, respectively. LPS administration induced significant increases in tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta and nitrate levels in blood serum with maximal levels observed at 1.5, 4, and 8 h after LPS administration, respectively. The effects of recombinant human lzactoferrin (rhLF) on LPS- induced alteration of gastrointestinal transit, and production of TNF-alpha, IL-1beta and nitrate were also studied. Animals were pretreated with rhLF 24 hours before intraperitoneal administration of LPS. RhLF significantly increased gastrointestinal transit during the lag phase. In addition, rhLF decreased the level of TNF-alpha in endotoxaemic animals. The levels of IL-1beta and nitrate were not significantly changed by rhLF. In conclusion, the effect of LPS on gastrointestinal transit is biphasic and the mechanism controlling the second phase most likely depends on TNF-alpha production, while the first phase most likely does not depend on TNF-alpha. On the other hand, it may be regulated by IL-1beta and nitric oxide production.

Animals↗
PubMedDate not supplied

Effects of fasting on evaluation of gastrointestinal transit with charcoal meal.

INTRODUCTION: At the present time, most studies investigating gastrointestinal transit time with charcoal are conducted in fasted rats. It seems reasonable to hypothesize that the fasting state of rats could influence the effect a compound had on gastrointestinal transit time. The purpose of this study was to investigate the effects of food on the pharmacological effects on gastrointestinal transit. METHODS: For each drug investigated, two sets of 32 male Sprague-Dawley rats were used. One set was studied after being fasted for approximately 6 h, the second set was studied after free access to food. Each set had 4 groups of animals (n=8/group) that were administered different doses, allowing the assessment of the drug effect after fasting and after free access to food. Animals were administered 0, 10, 25, and 75 mg/kg of morphine; 0, 10, 20, and 40 mg/kg loperamide, or 0, 0.05, 0.5, and 3.0 mg/kg clonidine. At predetermined times, an activated charcoal suspension was administered by oral gavage. Thirty minutes after receiving the charcoal meal, rats were euthanized and the small intestine was removed. The length of the small intestine and the distance traveled by the charcoal were recorded. For each animal, gastrointestinal transit was calculated as the percentage of the distance traveled relative to the total length of the small intestine. RESULTS: Baseline (vehicle dosed animals) gastrointestinal transit was significantly greater in fasted versus fed rats. In fasted rats, morphine did not have a significant effect on transit. In fed rats, 25 and 75 mg/kg morphine caused a significant decrease in transit. In fed and fasted rats, 0.5 and 3 mg/kg clonidine caused a significant decrease in transit. Loperamide did not affect gastrointestinal transit in fed or fasted rats at doses up to 40 mg/kg. DISCUSSION: These data demonstrate that food does not reduce the sensitivity of the gastrointestinal transit time.

Animals↗
PubMed2006

Effect of explosive noise on gastrointestinal transit and plasma levels of polypeptide hormones.

AIM: To investigate the effect of firing noise on gastrointestinal transit and probe its mechanism by measuring the levels of plasma polypeptide hormones. METHODS: A total of 64 SD rats were randomly divided into a control group and three stimulating groups. Firing noise of different intensity by sub-machine guns was used as inflicting factor. The effect of firing noise on liquid substance gastrointestinal transit and solid substance gastrointestinal transit was observed by measuring the ratio of carbon powder suspension transmitting and barium sticks transmitting respectively. Plasma levels of polypeptide hormones were measured by radio-immunoassay. RESULTS: The noise accelerated gastrointestinal transit of solid food by more than 80 db;and accelerated gastrointestinal transit of liquid food significantly by more than 120 db. Meantime, plasma levels of plasma motilin (MTL)(157.47+/-16.08; 151.90+/-17.08), somatostatin (SS)(513.97+/-88.77; 458.25+/-104.30), substance P (SP)(115.52+/-20.70; 110.28+/-19.96) and vasoactive intestinal peptide (VIP) (214.21+/-63.17; 251.76+/-97.24) remarkably changed also. CONCLUSION: Within a certain intensity range, the firing noise changes the levels of rat plasma gastrointestinal hormones, but the gastrointestinal transit is still normal. Beyond the range, the noise induces plasma hormone levels disturbance and gastrointestinal transit disorder.

Animals↗
PubMedDate not supplied

The effect of chilli on gastrointestinal transit.

The effects of chilli on gastrointestinal transit (gastric emptying, orocaecal transit, whole gut transit) were evaluated in eight healthy volunteers. In each subject, gastrointestinal transit of a standard test meal was measured on two separate days. On one of these occasions, 20 g of chilli powder was added to the meal. Gastric emptying was quantified with a radioisotopic technique, orocaecal transit by measurement of breath hydrogen concentrations and whole gut transit by counting the number of radio-opaque markers in the stool. The rate of gastric emptying was slower (P less than 0.05) and whole gut transit was faster (P less than 0.02) after the meal containing chilli, compared with the other meal. There was no significant difference in orocaecal transit. These results show that ingestion of chilli is associated with significant effects on gastric emptying and intestinal transit.

Adult↗
PubMed2005

Effect of N-methyl-d-aspartate receptor blockade on neuronal plasticity and gastrointestinal transit delay induced by ischemia/reperfusion in rats.

Intestinal ischemia impairs gastrointestinal motility. The aims of this study were to investigate the effect of intestinal ischemia on gastrointestinal transit and on the expression of enteric transmitters in the rat, and whether the glutamate N-methyl-d-aspartate receptors influence these effects. Ischemia (1 h), induced by occluding the superior mesenteric artery, was followed by 0 or 24 h of reperfusion. Normal and sham-operated rats served as controls. Serosal blood flow was measured with laser Doppler flow meter. Gastrointestinal transit was measured as time of appearance of a marker in fecal pellets. Immunohistochemistry was used to evaluate the number of neurons immunoreactive for neuronal nitric oxide synthase (NOS) or vasoactive intestinal polypeptide and the density of substance P immunoreactive fibers in the myenteric plexus. The N-methyl-d-aspartate receptors antagonist, (+)-5-methyl-10,11-dihydro-5HT-[a,b] cyclohepten-5,10-imine (MK-801) (1 mg/kg i.v.) or the NOS inhibitor, N-nitro-l-arginine (10 mg/kg i.v.) was administered prior to ischemia. Serosal blood flow was decreased by 70% during ischemia, but it was not altered in sham-operated rats. Gastrointestinal transit was significantly prolonged in ischemic/reperfused rats compared with controls. There was a significant increase in the number of vasoactive intestinal polypeptide and neuronal nitric oxide synthase immunoreactive neurons, and a marked decrease of substance P immunoreactive fibers in ischemia followed by 24 h of reperfusion animals compared with controls. These alterations were not observed in ischemia without reperfusion. A significant delay of gastrointestinal transit and increase of vasoactive intestinal polypeptide neurons were also observed in sham-operated rats. The changes in transmitter expression and gastrointestinal transit in ischemic/reperfused rats were prevented by pre-treatment with the NOS inhibitor, N-nitro-l-arginine or the N-methyl-d-aspartate receptors antagonist, MK-801. This study suggests an involvement of the glutamatergic system and its interaction with nitric oxide in intestinal ischemia/reperfusion. Ischemia/reperfusion might induce local release of glutamate that activates N-methyl-d-aspartate receptors leading to increased production of nitric oxide and adaptive changes in enteric transmitters that might contribute to gastrointestinal dysmotility.

Analysis of Variance↗
PubMed1986

Effects of ethanol on gastrointestinal transit in mice.

The acute effects of ethanol on gastrointestinal transit were studied in mice. Intraperitoneal injection of 2 or 3 g of ethanol/kg had a dose-dependent inhibitory effect on gastrointestinal transit. Subcutaneous injection of 4 g of ethanol/kg also inhibited gastrointestinal transit, but this route was less effective than the intraperitoneal route of administration. Further examination of both the time course of inhibition and the weight of the stomach contents suggested that intraperitoneal injections of moderate doses of ethanol did not alter gastric emptying. The data indicated that gastrointestinal transit is inhibited by ethanol and that the most sensitive locus is the small intestine rather than the stomach.

Animals↗
PubMed1986

Centrally administered bombesin affects gastrointestinal transit and colonic bead expulsion through supraspinal mechanisms.

Effects of bombesin on gastrointestinal transit and colonic bead expulsion (CBE) were studied in male, ICR mice. Mice received graded doses of bombesin or saline by either the i.c.v., intrathecal (i.t.) or i.p. routes; morphine was studied as the reference compound. Both compounds slowed gastrointestinal transit in a dose-dependent manner by these routes. Intracerebroventricular bombesin was 13.5 and 3406 times more potent than the i.t. and i.p. peptide, respectively. Intracerebroventricular or i.t. bombesin or morphine also produced dose-related inhibition of CBE. Intracerebroventricular bombesin was 1.54 times more potent than i.t. bombesin, whereas i.p. bombesin at doses 11,000 times greater (10 micrograms/kg; 25-g mouse) had no effect on CBE. Gastrointestinal transit and CBE were also studied in spinally transected (second thoracic vertebra) mice in which brain-spinal cord communication (neural and cerebrospinal fluid) had been interrupted. Cord transection eliminated the inhibition of gastrointestinal transit by i.t., but not i.c.v., bombesin. In contrast, morphine was effective by either route in normal or spinally transected mice. The CBE effects of i.t., but not i.c.v., bombesin were eliminated by spinal transection, whereas morphine was still effective by either the i.c.v. or i.t. route. These results suggest that 1) centrally administered bombesin acts at a central site to produce inhibition of gastrointestinal transit and CBE, 2) morphine inhibits gastrointestinal transit and CBE at both spinal or supraspinal sites, independent of an intact brain-cord axis and 3) i.t., but not i.c.v., bombesin requires communication between these two central sites. Intrathecal bombesin requires activation of supraspinal sites to produce its gut effects.

Animals↗
PubMedDate not supplied

Studies on the mechanism of thyrotropin releasing hormone induced inhibition of gastrointestinal transit.

Intracerebral administration of thyrotropin releasing hormone (TRH) inhibited gastrointestinal transit in the mouse as determined by the charcoal meal test. A similar inhibitory effect was produced by morphine administered subcutaneously. TRH enhanced morphine-induced inhibition of gastrointestinal transit. Intracerebral injections of cyclo (His-Pro), a postulated metabolite, did not affect gastrointestinal transit either by itself or that produced by morphine. It is suggested that gastrointestinal transit effects of TRH are not mediated via its conversion to cyclo (His-Pro).

Animals↗
PubMed1999

Quinine-induced inhibition of gastrointestinal transit in mice: possible involvement of endogenous opioids.

The effect of quinine, a cinchona alkaloid, was studied on gastrointestinal transit in mice. Intraperitoneal (i.p.) administration of quinine inhibited the intestinal propulsion of a charcoal suspension at a dose of 100 mg/kg, comparing favorably with 5 mg/kg morphine. In an attempt to probe into the mechanism underlying this inhibition, a possible modulation by minoxidil (1 mg/kg, p.o.) and glibenclamide (1 mg/kg, p.o.), the drugs that, respectively, open and close ATP-sensitive K+ channels was tested on gastrointestinal transit in animals treated or not with quinine or morphine. While minoxidil produced no significant change of normal transit, glibenclamide significantly increased it. However, both drugs blocked the quinine-induced reduction in gastrointestinal transit. In contrast, the inhibitory effect of morphine on gastrointestinal transit was not modified by either drug. The effects of quinine as well as of morphine on gastrointestinal transit were significantly antagonized by naloxone (2 mg/kg, s.c.), a mu-opioid receptor antagonist but not by yohimbine (1 mg/kg, i.p.), an alpha2-adrenoceptor antagonist. Furthermore, quinine at a lower dose (25 mg/kg) that showed no per se effect on gastrointestinal transit, significantly potentiated the response to 2.5 mg/kg morphine. Although the role of ATP-sensitive K+ channels in the action of quinine and morphine was not clarified by the present results, a possible involvement of endogenous opioid(s) in the quinine-induced inhibition of gastrointestinal transit can be suggested.

Adenosine Triphosphate↗
PubMed2002

Gastrointestinal transit in relation to gut endocrine cells in animal models of human diabetes.

Gastrointestinal transit was measured in non-obese diabetic (NOD) mice, as an animal model of human diabetes type 1, and in obese diabetic mice, as an animal model of human diabetes type 2. The endocrine cells known to correlate to gastrointestinal transit, namely secretin, serotonin, Peptide YY (PYY) and enteroglucagon cells, were identified by immunocytochemistry and quantified by computer image analysis in different segments of the gut. Gastrointestinal transit was significantly accelerated in NOD mice and slower in obese diabetic mice than in controls. The density of duodenal secretin and serotonin as well as colonic PYY and enteroglucagon cells in NOD mice was significantly higher than that of control mice. On the other hand, the density of duodenal secretin and serotonin cells was significantly lower in obese diabetic mice than in controls. It was concluded that changes in duodenal secretin and colonic serotonin, PYY and enteroglucagon cells may play a role in accelerated gastrointestinal transit in NOD mice and delayed gastrointestinal transit in obese diabetic mice.

Animals↗
PubMed1988

Evidence for a peripheral action of thyrotropin releasing hormone on gastrointestinal transit in mice.

The effect of the two analogs of thyrotropin-releasing hormone (TRH), namely MK-771 and DN-1417, administered peripherally, on the actions of morphine and loperamide on gastrointestinal transit, was investigated in mice. The actions of naltrexone and methyl naltrexone on these effects were also determined in order to assess the central or peripheral mechanism of action. The administration of morphine sulfate (5 mg/kg) inhibited gastrointestinal transit, as measured by the charcoal meal test. The effect of morphine was potentiated by MK-771 and DN-1417 at the 10 mg/kg dose. The peripheral administration of DN-1417 inhibited gastrointestinal transit but MK-771 had no effect. Naltrexone antagonized the potentiating effect of the peptides on the effect of morphine on gastrointestinal transit. Methyl naltrexone, which crosses the blood-brain barrier with difficulty, also antagonized the potentiating effect of the peptides on the action of morphine on gastrointestinal transit. A subthreshold dose (0.5 mg/kg) of loperamide, a peripherally acting opiate, which had no effect on gastrointestinal transit by itself, when combined with MK-771 or DN-1417 significantly inhibited gastrointestinal transit. The administration of methyl naltrexone had little effect on loperamide-induced inhibition of gastrointestinal transit but antagonized the potentiating effect of MK-771 and DN-1417. It is concluded that the effects of analogs of thyrotropin releasing hormone on gastrointestinal transit involve peripheral sites of action, the effect of DN-1417 was not antagonized by naloxone and that the inhibitory effect of DN-1417 on gastrointestinal transit is not mediated by opiate receptors.

Animals↗