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PubMed1984

Comparative effects of prolyl-leucyl-glycinamide and naloxone on morphine-induced inhibition of gastrointestinal transit.

The effects of prolyl-leucyl-glycinamide (MIF) and naloxone on the gastrointestinal transit in mice were investigated using the charcoal meal test. MIF administered intraperitoneally (IP) (1-10 mg/kg) or intracerebroventricularly (ICV) (10 micrograms/mouse) had no effect on the transit. Administration of morphine by subcutaneous (SC) route significantly inhibited the gastrointestinal transit. The morphine-induced inhibition of the transit was not affected by MIF whether given by IP or ICV route. Administration of the opiate antagonist naloxone (1 mg/kg, IP or 10 micrograms/mouse, ICV) had no effect on the gastrointestinal transit, but it significantly antagonized the inhibition produced by morphine. Some earlier studies have indicated narcotic antagonistic effect of MIF. However, in the present study, evidence for such an action of MIF was not obtained. It is suggested that MIF does not appear to have narcotic antagonistic activity and further supports an earlier study from this laboratory that MIF may not interact with opiate receptors.

Animals↗
PubMed1994

Magnetic markers as a noninvasive tool to monitor gastrointestinal transit.

A novel method to monitor gastrointestinal transit of solid oral dosage forms or nutrients is presented, providing a simultaneous recording of gastrointestinal motility of the traversed section. Based on the measurement of the magnetic field of an ingested magnetized marker, its location is found by fitting a magnetic dipole field to the measured data.

Gastrointestinal Motility↗
PubMedDate not supplied

Influence of pregnancy and uterine weight on rat gastrointestinal transit.

Orogastric feeding of a charcoal meal to rats was employed to measure whether the various stages of pregnancy could influence gastrointestinal transit. The oestrous cycle of female Sprague-Dawley rats was checked daily. If pro-oestrus occurred, the first day of pregnancy was defined to be on the next day after the copulation. Gastrointestinal transit studies were conducted on day 7 (first trimester), day 14 (second) and day 21 (third), respectively. The rats were killed 15 min after the successful feeding of a calorie-free, charcoal-containing test meal via a transiently placed orogastric catheter. Gastrointestinal transit was defined as the per cent of charcoal transit divided by the total length of the small intestine. These results were compared with the data obtained from non-pregnant female rats. Mean percentages of transit for the first, second and third trimester, and for controls were 42.8 +/- 1.9, 45.3 +/- 4.1, 35.7 +/- 1.7 and 42.6 +/- 1.4%, respectively (mean +/- s.e.). Late pregnancy elicited a marked inhibition of transit (P < 0.01). A significant negative correlation between transit and uterine weight of all pregnant rats was seen (r = -0.50, P < 0.05). The present study indicates that inhibited gastrointestinal transit occurs in the late pregnant rat.

Animals↗
PubMed1995

Effects of sex steroid hormones on gastric emptying and gastrointestinal transit in rats.

In vitro studies have shown that estrogen and progesterone can affect the contractile response and myoelectric activity of the gastrointestinal smooth muscle. The present study was designed to investigate the effect of sex steroid hormones on gastric emptying and gastrointestinal transit were assessed in rats 15 min after intragastric instillation of a test meal containing charcoal and 51Cr. Gastric emptying was determined by measuring the amount of labeled chromium contained in the small intestine as a percentage of the initial amount received. Gastrointestinal transit was evaluated by calculating both the geometric center of distribution of the radiolabeled marker and the charcoal transit in the intestine. The experimental animals included diestrus rats; ovariectomized rats treated with vehicle, estradiol, and/or progesterone; and normal male and orchiectomized rats treated with vehicle or testosterone. Female rats in diestrus had a slower gastric emptying and a lesser geometric center value than ovariectomized rats. Estradiol inhibited gastric emptying but did not affect gastrointestinal transit. Progesterone increased gastric emptying. Progesterone at lower dose (10 mg/kg) decreased the geometric center compared with higher doses (20 or 40 mg/kg) or vehicle controls. A mixture of estradiol (10 micrograms/kg) and progesterone (20 mg/kg) inhibited gastric emptying to a similar degree as estradiol (10 micrograms/kg) did. Testosterone had no influence on gastric emptying or gastrointestinal transit. These results suggest that estradiol and a mixture of estradiol and progesterone inhibit, whereas progesterone enhances, gastric emptying. Testosterone did not play a role in gastrointestinal motility.

Animals↗
PubMed1995

Potentiation of intrathecal DAMGO antinociception, but not gastrointestinal transit inhibition, by 5-hydroxytryptamine and norepinephrine uptake blockade.

Spinally administered mu opioid agonists produce potent antinociception and inhibition of gastrointestinal transit. Blockade of 5-hydroxytryptamine (5-HT) or norepinephrine (NE) uptake potentiates intrathecal (i.t.) DAMGO antinociception. To determine whether 5-HT and NE uptake blockade will also potentiate the gastrointestinal inhibition, mice were treated with zimelidine, desipramine or saline, followed by i.t. DAMGO and tested for tailflick antinociception or inhibition of gastrointestinal transit. DAMGO produced antinociception dose-dependently (ED50 = 4.6 ng). Zimelidine (10 mg/kg, s.c., 1 hr before DAMGO) produced a 6.2-fold leftward shift in the antinociceptive dose-response curve (ED50 = 0.73 ng). Desipramine produced a 5.3-fold shift (ED50 = 1.4 ng). DAMGO also produced a dose-dependent inhibition of gastrointestinal transit (ED50 = 117 ng). However, zimelidine or desipramine treatment did not affect DAMGO inhibition of gastrointestinal transit (ED50 = 80 ng.).

Animals↗
PubMed1982

[Gastrointestinal transit in the chicken using 198Au-colloid as a marker (author's transl)].

Gastrointestinal transit in the chicken was investigated by using 198Au-colloid as a marker. Gastrointestinal transit was determined following administration of a 198Au-colloid solution (370 kBq (10 microCi), 0.5 ml) into the proventriculus by measuring the distribution of radioactivity in the gastrointestine. Most of 198Au-colloid administered into the proventriculus was transferred instantly to the gizzard and subsequently, some part of it quickly to the duodenum and the upper segment of the jejunoileum. A considerable quantity of 198Au-colloid in the duodenum, the upper and middle segment of the jejunoileum regurgitated to the gizzard. 198Au-colloid transferred to the caecum was retained for a long time (more than 48 hours) in these segments. A part of 198Au-colloid was found in the feces 90 to 120 minutes after administration into the proventriculus and the greater part of it was excreted into the feces 24 to 48 hours. Subcutaneous administration of acetylcholine (2 mg/kg) increased the gastrointestinal transit but atropine (2 mg/kg) decreased.

Acetylcholine↗
PubMed2006

Inducible nitric oxide synthase and tumor necrosis factor-alpha in delayed gastric emptying and gastrointestinal transit induced by lipopolysaccharide in mice.

Gastrointestinal motility disturbances during endotoxemia are probably caused by lipopolysaccharide (LPS)-induced factors: candidates include nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha), interleukin-1ss, and interleukin-6. Flow cytometry was used to determine the effects of LPS and these factors on gastric emptying (evaluated indirectly by determining percent gastric retention; %GR) and gastrointestinal transit (GIT) in male BALB/c mice (23-28 g). NO (300 microg/mouse, N = 8) and TNF-alpha (2 microg/mouse, N = 7) increased (P < 0.01) GR and delayed GIT, mimicking the effect of LPS (50 microg/mouse). During early endotoxemia (1.5 h after LPS), inhibition of inducible NO synthase (iNOS) by a selective inhibitor, 1400 W (150 microg/mouse, N = 11), but not antibody neutralization of TNF-alpha (200 microg/mouse, N = 11), reversed the increase of GR (%GR 78.8 +/- 3.3 vs 47.2 +/- 7.5%) and the delay of GIT (geometric center 3.7 +/- 0.4 vs 5.6 +/- 0.2). During late endotoxemia (8 h after LPS), both iNOS inhibition (N = 9) and TNF-alpha neutralization (N = 9) reversed the increase of GR (%GR 33.7 +/- 2.0 vs 19.1 +/- 2.6% (1400 W) and 20.1 +/- 2.0% (anti-TNF-alpha)), but only TNF-alpha neutralization reversed the delay of GIT (geometric center 3.9 +/- 0.4 vs 5.9 +/- 0.2). These findings suggest that iNOS, but not TNF-alpha, is associated with delayed gastric emptying and GIT during early endotoxemia and that during late endotoxemia, both factors are associated with delayed gastric emptying, but only TNF-alpha is associated with delayed GIT.

Animals↗
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↗
PubMed1999

Complete cervical or thoracic spinal cord transections delay gastric emptying and gastrointestinal transit of liquid in awake rats.

STUDY DESIGN: To determine the changes on gastric emptying and gastrointestinal transit of liquid throughout the first week after spinal cord transection (SCT) in rats. METHODS: Male Wistar rats (n=121) were fasted for 16 h and a complete SCT or laminectomy was performed between C7 and T1 (cervical group) or between T4 and T5 (thoracic group). Dye recovery in the stomach, proximal, mid and distal small intestine was determined 30 min, 6 h, 1, 3 or 7 days after surgery. The test meal (1.5 ml of a phenol red solution, 0.5 mg/ml in 5% glucose) was intragastrically administered and the animals sacrificed by cervical dislocation 10 min later. RESULTS: Cervical SCT increased dye recovery in the stomach (P<0.05) by 70.1, 78.7, 34.2, 41.3 and 50.9% while it decreased recovery in the mid small intestine (P<0.05) by 87.1, 85.1, 74.8, 59.5 and 80.1%, respectively 30 min, 6 h, 1, 3 and 7 days after SCT. Thoracic SCT increased gastric recovery (P<0.05) by 43.5, 67.6, 51.2, 75.4 and 38. 9% while it decreased recovery in the mid small intestine (P<0.05) by 100, 100, 45.6, 100 and 66.6%, respectively 30 min, 6 h, 1, 3 and 7 days after SCT. A separate group was submitted to laminectomy+bilateral sciatic nerve transection (paraplegic sham). Gastric emptying and gastrointestinal transit were not inhibited in this group. CONCLUSION: In summary, gastric emptying and gastrointestinal transit of liquid are inhibited throughout the first week after high SCT in awake rats.

Animals↗
PubMed2006

Involvement of mu-opioid receptors in antinociception and inhibition of gastrointestinal transit induced by 7-hydroxymitragynine, isolated from Thai herbal medicine Mitragyna speciosa.

7-hydroxymitragynine, a constituent of the Thai herbal medicine Mitragyna speciosa, has been found to have a potent opioid antinociceptive effect. In the present study, we investigated the mechanism of antinociception and the inhibitory effect on gastrointestinal transit of 7-hydroxymitragynine, and compared its effects with those of morphine. When administered subcutaneously to mice, 7-hydroxymitragynine produced antinociceptive effects about 5.7 and 4.4 times more potent than those of morphine in the tail-flick (ED50=0.80 mg/kg) and hot-plate (ED50=0.93 mg/kg) tests, respectively. The antinociceptive effect of 7-hydroxymitragynine was significantly blocked by the mu1/mu2-opioid receptor antagonist beta-funaltrexamine hydrochloride (beta-FNA) and the mu1-opioid receptor-selective antagonist naloxonazine in both tests. Thus, 7-hydroxymitragynine acts predominantly on mu-opioid receptors, especially on mu1-opioid receptors. Isolated tissue studies further supported its specificity for the mu-opioid receptors. Further, 7-hydroxymintragynine dose-dependently (ED50=1.19 mg/kg, s.c.) and significantly inhibited gastrointestinal transit in mice, as morphine does. The inhibitory effect was significantly antagonized by beta-FNA pretreatment, but slightly antagonized by naloxonazine. The ED50 value of 7-hydroxymitragynine on gastrointestinal transit was larger than its antinociceptive ED50 value. On the other hand, morphine significantly inhibits gastrointestinal transit at a much smaller dose than its antinociceptive dose. These results suggest that mu-opioid receptor mechanisms mediate the antinociceptive effect and inhibition of gastrointestinal transit. This compound induced more potent antinociceptive effects and was less constipating than morphine.

Analgesics↗
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↗
PubMed1995

Orally administered opioid antagonists reverse both mu and kappa opioid agonist delay of gastrointestinal transit in the guinea pig.

Kappa(kappa) opioid agonists slow gastrointestinal transit in the guinea pig and the mouse but not the rat. Opioid antagonists naloxone and naltrexone are mu (mu) preferring, while the antagonist nalmefene has more kappa binding activity. When administered orally, the specific opioid antagonists naloxone, naltrexone, and nalmefene are able to reverse the gastrointestinal transit delay caused by orally administered mu and kappa opioid agonists (morphine and U-50, 488H) in a dose dependent fashion as measured by the leading edge of charcoal meal in the guinea pig. Oral naltrexone and nalmefene have significantly more central nervous system (CNS) bioavailability than oral naloxone. However, orally administered naloxone was as effective as either naltrexone or nalmefene in reversing mu opioid agonist induced orocecal transit delays (single agonist dose apparent ED50s = 12.3 +/- 4, 7.3 +/- 4, and 13.5 +/- 6 mg/kg respectively). Nalmefene was more active than either naltrexone or naloxone in its ability to reverse the kappa agonist U-50,488H (single agonist dose apparent ED50s = 18.3 +/- 12*, 37.5 +/- 5, and 61.9 +/- 5 mg/kg respectively; * = p < 0.05). These data confirm the enteric action of orally administered opioids and further supports our earlier findings of the presence of kappa opioid activity in the guinea pig enteric nervous system.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed2006

Endothelin ETA receptor blockade potentiates morphine analgesia but does not affect gastrointestinal transit in mice.

Development of analgesic tolerance and constipation remain a major clinical concern during long-term administration of morphine in pain management. Central endothelin mechanisms are involved in morphine analgesia and tolerance. The present study was conducted to investigate the effect of intracerebroventricular (i.c.v.) and peripheral administration of endothelin ET(A) receptor antagonist, BMS182874, and endothelin ET(B) receptor agonist, IRL1620, on morphine analgesia and changes in gastrointestinal transit in male Swiss Webster mice. Results indicate that morphine (6 mg/kg, s.c.) produced a significant increase in tail flick latency compared to control group. Pretreatment with BMS182874 (50 microg, i.c.v.) significantly enhanced morphine-induced analgesia, while IRL1620 (30 microg, i.c.v.) pretreatment did not affect tail-flick latency values. Changes in gastrointestinal transit were measured by percent of distance traveled by charcoal in the small intestine of gastrointestinal tract. Percent distance traveled in morphine (6 mg/kg, s.c.) treated mice (48.45+/-5.65%) was significantly lower (P<0.05) compared to control group (85.07+/-1.82%). Administration of BMS182874 centrally (50 mug, i.c.v.) or peripherally (10 mg/kg, i.p.) did not affect morphine-induced inhibition of gastrointestinal transit. Pretreatment with IRL1620 (30 microg, i.c.v., or 10 mg/kg, i.v.) also did not affect morphine-induced inhibition of gastrointestinal transit. This study demonstrates that endothelin ET(A) receptor antagonists delivered to the CNS enhance morphine analgesia without affecting gastrointestinal transit.

Analgesics, Opioid↗
PubMed1995

Effect of diabetes on the morphine-induced inhibition of gastrointestinal transit.

The effect of diabetes on the morphine-induced inhibition of gastrointestinal transit was examined in mice. Morphine dose-dependently inhibited gastrointestinal transit after s.c. administration in both non-diabetic mice and diabetic mice. There was no significant difference between the ED50 values for this antitransit effect of morphine in non-diabetic and diabetic mice. The gastrointestinal antitransit effect of morphine was significantly antagonized by pretreatment with beta-funaltrexamine (40 mg/kg, s.c.), a selective mu-opioid receptor antagonist, in both non-diabetic and diabetic mice. However, pretreatment with naloxonazine (35 mg/kg, s.c.), a selective mu 1-opioid receptor antagonist, had no effect on the antitransit properties of morphine. These results suggest that diabetes failed to alter the mu 2-opioid receptor-mediated antitransit effect of morphine.

Animals↗
PubMed2001

In vivo evidence that protease-activated receptors 1 and 2 modulate gastrointestinal transit in the mouse.

1. Protease-activated receptors (PARs) 1 and 2 modulate the gastric and intestinal smooth muscle motility in vitro. In the present study, we examined if activation of PAR-2 and PAR-1 could alter gastrointestinal transit in mice. 2. Intraperitoneal administration of the PAR-2-activating peptide SLIGRL-NH(2), but not the inactive control LSIGRL-NH(2), at 1 - 5 micromol kg(-1), in combination with the aminopeptidase inhibitor amastatin at 2.5 micromol kg(-1), facilitated gastrointestinal transit in a dose-dependent manner. The human PAR-1-derived peptide SFLLR-NH(2) and the specific PAR-1 agonist TFLLR-NH(2), but not the inactive control FSLLR-NH(2), at 2.5 - 10 micromol kg(-1), in combination with amastatin, also promoted gastrointestinal transit. 3. The Ca2+-activated, small conductance K+ channel inhibitor apamin at 0.01 micromol kg(-1) significantly potentiated the actions of SLIGRL-NH(2) and TFLLR-NH(2) at subeffective doses. 4. The increased gastrointestinal transit exerted by either SLIGRL-NH(2) at 5 micromol kg(-1) or TFLLR-NH(2) at 10 micromol kg(-1) was completely abolished by the L-type Ca2+ channel inhibitor verapamil at 61.6 micromol kg(-1). In contrast, the tyrosine kinase inhibitor genistein at 18.5 micromol kg(-1) failed to modify the effects of the agonists for PAR-2 or PAR-1. 5. These findings demonstrate that PAR-1 and PAR-2 modulate gastrointestinal transit in mice in vivo. Our data also suggest that the PAR-1-and PAR-2-mediated effects are modulated by apamin-sensitive K+ channels and are dependent on activation of L-type Ca2+ channels, but independent of tyrosine kinase. Our study thus provides novel evidence for the physiological and/or pathophysiological roles of PARs 1 and 2 in the digestive systems, most probably during inflammation.

Amino Acid Sequence↗
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↗
PubMed1982

Effect of pregnancy on gastrointestinal transit.

In order to evaluate the possible effects of pregnancy-associated sex steroids on gastrointestinal function, we determined gastrointestinal transit times and sex steroid levels in 15 women during the third trimester of their pregnancies and again 4--6 weeks following delivery when gastrointestinal function had symptomatically returned to normal. Gastrointestinal transit time from ingestion of a liquid lactulose meal to its delivery to the cecum was determined by monitoring breath hydrogen concentrations at 10-min intervals. Gastrointestinal transit times were significantly prolonged in the third trimester of pregnancy, when progesterone and estradiol levels were increased, compared to the postpartum period. This study supports previous findings which suggest that increasing levels of progesterone and estradiol affect gastrointestinal function and therefore may contribute to gastrointestinal symptoms that often occur in pregnant women.

Adult↗
PubMedDate not supplied

The effect of thyrotropin releasing hormone and morphine on gastrointestinal transit.

The effect of thyrotropin releasing hormone (TRH) alone and in combination with morphine on the gastrointestinal transit was investigated by using the charcoal meal test in mice. The intraperitoneal (IP) administration of TRH decreased the transit when given in a dose of 1.0 mg/kg 10 min prior to the meal. The intracerebroventricular (ICV) administration of TRH (10 micrograms/mouse) also inhibited the transit when given just prior to the charcoal meal. Subcutaneous (SC) administration of morphine (5, 10 and 20 mg/kg) inhibited gastrointestinal transit in a dose dependent manner. When TRH (1,3 and 10 mg/kg, IP as well as 0.3 microgram, ICV) which had no effect on the transit by itself was combined with morphine (10 mg/kg, SC), an enhancement in the inhibition of the transit was observed. TRH-induced inhibition of the transit was antagonized by naloxone (0.1 mg/kg, SC). It is concluded that TRH inhibits gastrointestinal transit in the mouse possibly via the opiate receptor system.

Animals↗