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At least 19 recordsLinked to original sources
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↗
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↗
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↗
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↗
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↗
PubMed1985

Stereospecific opiate receptors in the actions of thyrotropin releasing hormone and morphine on gastrointestinal transit.

Studies in these laboratories have shown that morphine and thyrotropin releasing hormone (TRH) inhibit gastrointestinal transit in the mouse. Administration of morphine sulfate (5 mg/kg, s.c.) or TRH (10 microgram i.c.v.) to mice inhibited gastrointestinal transit as measured by the charcoal meal test. In order to determine whether the effects of TRH and morphine were mediated via stereospecific opiate receptors, the effects of two stereoisomers of an antagonist, (-) alpha -5,9-diethyl-2'-hydroxy-2-(3-furylmethyl)6,7-benzomorphan (MR2266), the active isomer and (+) alpha-5,9-diethyl-2'-hydroxy-2-(3-furylmethyl)6,7-benzomorphan (MR 2267), the inactive isomer, on morphine and TRH induced changes in gastrointestinal transit were determined. Morphine and THR induced inhibition of gastrointestinal transit was antagonized by MR 2266 (1 and 3 mg/kg, s.c.) but was unaffected by MR 2267. These studies provide evidence for the involvement of opiate receptors in the actions of morphine and TRH on gastrointestinal transit, and further suggest that the receptors are stereospecific in nature.

Animals↗
PubMed1988

Calcitonin and CGRP inhibit gastrointestinal transit via distinct neuronal pathways.

This study compares the central nervous system effects of rat calcitonin and rat calcitonin gene-related peptide (CGRP) on gastrointestinal transit in freely moving rats. Calcitonin and CGRP (0.01-1.0 nmol) injected into the lateral cerebral ventricle significantly inhibited gastric emptying and small bowel transit but did not affect large bowel transit. These biological actions were abolished by ganglionic blockade with chlorisondamine but not by noradrenergic blockade with bretylium. Truncal vagotomy abolished the inhibitory effects of CGRP but not those of calcitonin. Neither adrenalectomy nor hypophysectomy prevented the inhibitory actions of calcitonin and CGRP on gastric emptying and small bowel transit. Intraperitoneal administration of calcitonin and CGRP (1 nmol) produced inhibition of gastric emptying only, and this was not abolished by ganglionic blockade. These results indicate that calcitonin and CGRP exhibit similar central nervous system effects, producing inhibition of gastric emptying and small bowel transit but not altering large bowel transit. Calcitonin inhibits gastrointestinal transit via nonvagal, nonnoradrenergic autonomic efferents, yet CGRP inhibits gastrointestinal transit via vagal efferent fibers.

Animals↗
PubMed1990

Fractional gastrointestinal transit time: intra- and interindividual variation.

The intra- and interindividual variation in the gastrointestinal transit times was measured in 12 healthy adult test subjects using a scintigraphic method with 111In marked single unit tablets. Test conditions were semi-standardized. The variation within the same individual was as large as the variation between different subjects regarding the transit times through both the small and the large intestines. The small intestine transit time was 5 h (median) with an interquartile range of 4-7 h. The median transit time through the large intestine was 23.5 h (interquartile range 19.0-40.5 h). The coefficient of repeatability for the small intestinal and large intestinal transit time was 4 h and 33 h respectively. Our conclusion is that the 111In single unit capsule method can be used for measuring the fractional gastrointestinal transit times, but the intra- and interindividual variations are rather large and similar. From a radiation-hygienic point of view the 111In single unit capsule method is acceptable. The large inter- and intraindividual variation in gastrointestinal transit time might be an important factor in the absorption of certain drugs.

Adult↗
PubMed1986

Vagotomy inhibits the effect of neurotensin on gastrointestinal transit in the rat.

Neurotensin has previously been shown to delay gastric emptying, gastrointestinal transit and ileo-caecal emptying in the rat. To investigate the vagal influence on these effects of neurotensin, separate groups of rats were operated with combined vagotomy and pyloroplasty or with pyloroplasty alone and compared to a group of normal rats. All animals were supplied with a permanent gastrointestinal catheter and a venous catheter. After operation the rats were allowed to recover for 7 days, and were fasted for 24 h prior to the experiments. A radioactive marker of 1.0-0.5 ml Na2(51)CrO4 in isotonic polyethylene glycol 400 was instilled intraluminally in the stomach, proximal or distal the small intestine. Saline (control animals) or neurotensin (test animals) was given i.v. in each group studied. The animals were killed at 15, 30, 60, and 120 min after administration of the marker. The distribution of the marker in the gastrointestinal tract was registered with a scintillation detector and quantitative analysis of the amount of radioactivity retained in separate gastrointestinal segments was carried out. Gastric emptying was delayed by combined vagotomy and pyloroplasty (P less than 0.01) compared to pyloroplasty alone and normals. Neurotensin at doses of 6 (P less than 0.05) and 12 (P less than 0.01) pmol kg-1 min-1 retarded gastric emptying dose-dependently in normals and rats with pyloroplasty alone, but did not further slow the gastric emptying in rats with vagotomy and pyloroplasty. However, at a dose of 24 pmol kg-1 min-1 neurotensin delayed gastric emptying (P less than 0.01) compared to controls. Gastrointestinal transit was slowed down by neurotensin at a dose of 6 pmol kg-1 min-1 in normals (P less than 0.01) and rats with pyloroplasty alone (P less than 0.05). In rats with vagotomy and pyloroplasty, neurotensin at doses of 6 and 12 pmol kg-1 min-1 had no effect on gastrointestinal transit.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

A tachykinin antagonist inhibits gastric emptying and gastrointestinal transit in the rat.

The effect of a substance P antagonist, [D-Pro2, D-Trp7,9]-substance P (SPA), on gastric emptying and gastrointestinal transit in the rat was studied in order to elucidate a possible physiological role of endogenous substance P and other tachykinins in gastrointestinal motility. SPA was given by intraperitoneal injection concurrently with the intragastric administration of a test meal containing charcoal and 51Cr. Examination 15 min after the test meal showed that SPA (0.13-1.3 mumol kg-1) inhibited gastric emptying and gastrointestinal transit in a dose-dependent manner. The inhibitory effect of SPA on gastric emptying and gastrointestinal transit remained unchanged after pretreatment of rats with mepyramine (8.7 mumol kg-1) plus cimetidine (19.8 mumol kg-1) or with guanethidine (67 mumol kg-1). Since a full examination of SPA as a specific tachykinin antagonist was not possible in vivo, SPA was also tested on circular muscle strips from the rat gastric corpus in vitro. Submaximal contractions in response to bombesin or bethanechol were not reduced by SPA (50 microM), whereas those in response to substance P were inhibited. The results suggest that SPA inhibits gastric emptying and gastrointestinal transit by interfering with the action of tachykinins released from enteric nerves and that endogenous tachykinins are involved in the regulation of gastrointestinal motility.

Animals↗
PubMed1991

[Gastrointestinal absorption of nitrofurantoin: evaluation of a newly developed method for determination of the gastrointestinal transit time in dogs].

The relationship between the oral absorption and gastrointestinal transit time of nitrofurantoin was investigated in dogs by the double-marker method using acetaminophen and salicylazosulfapyridine as markers. The extent of bioavailability of nitrofurantoin gave correlations with both gastric emptying time and small intestinal transit time. The results indicate that the slower the passage from the stomach into the small intestine and/or the longer the residence time in the small intestine, the oral absorption efficiency of nitrofurantoin increases. These observations were consistent with the reported findings from in situ absorption study in rats and intestinal intubation study in humans, respectively. Moreover, it was clarified that small intestinal transit time is the most important determinant of absorption of nitrofurantoin, since the good correlation was observed between the small intestinal transit time and the extent of bioavailability. The double-marker method appears consequently to be useful tool for the determination of the gastrointestinal transit time in dogs.

Animals↗
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↗
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↗
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↗
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↗