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PubMedDate not supplied

Gastrointestinal transit in nonobese diabetic mouse: an animal model of human diabetes type 1.

Gastrointestinal transit (GI) in the nonobese diabetic (NOD) mouse, an animal model of human diabetes type 1, was examined in animals with short- (duration 1-5 days) and long-term (duration 28-35 days) diabetes. Blood glucose level, serum insulin concentration, and gut neuroendocrine peptide content were also measured. GI was significantly rapid in NOD mice with long-term diabetes (LTD), but was not correlated with blood glucose level, serum insulin concentration, or pancreatic insulin content. GI was correlated with duodenal secretin content, but not with the content of other neuroendocrine peptides in the different segments investigated. Whereas antral vasoactive intestinal peptide (VIP) content in NOD mice with LTD was significantly higher, colonic VIP was lower in NOD mice with short-term diabetes (STD). In the duodenum, whereas the concentration of secretin in NOD mice with both STD and LTD was lower, the gastrin content was higher. Duodenal somatostatin content in NOD mice with LTD was lower. In colon, the content of galanin in NOD mice with LTD was higher than in controls. The decreased content of secretin may be among the factors that cause rapid GI in NOD mice with LTD. Changes in the antral content of VIP, duodenal somatostatin, and colonic galanin in NOD mice with LTD may cause low intestinal secretion and, together with rapid GI, give rise to diarrhoea, which is a common symptom in diabetes.

Animals↗

PubMed1981

Measurement of gastrointestinal transit of solid food using a colestipol-phenol red complex as a marker.

The present study was undertaken to determine whether colestipol-phenol red complexes can be used as markers for gastrointestinal transit of solid food. Colestipol (1.0g) bound completely with phenol red (10 mg) to form a stable complex in water (pH 7.0) Phenol red was more readily eluted from colestipol with 20 ml of 1 N HCl than 1 N NaOH, but was not eluted with 0.1 N HCL (pH 1.0). It was therefore assumed that the complex would remain stable in the gastrointestinal tract. Also, phenol red in the gastrointestinal tract was quantitatively eluted from the complex with 20 ml of 1N HCl. In a study on gastric emptying, phenol red solution (liquid food) was excreted from the stomach in a zero-order manner, and the colestipol-phenol red complex (solid food) in a first-order manner. It was concluded that colestipol-phenol red complexes can be used as markers of gastrointestinal transit.

Animals↗

PubMed1982

Effects of dermorphin on gastrointestinal transit in rats.

The effects of subcutaneous (s.c.) and intracerebroventricular (i.c.v.) injections of dermorphin on gastric emptying and intestinal transit were studied in rats. Dermorphin injected i.c.v. delayed gastric emptying and this effect was dose-dependent. I.c.v. injections of dermorphin also inhibited intestinal transit but a dose level 5 to 10 times higher than that active on gastric emptying was required. Subcutaneous injections of dermorphin also inhibited gastrointestinal transit but inhibition of the two functions never exceeded 60%. The effect of i.c.v. and s.c. doses of dermorphin was antagonized by a 1 mg . kg-1 dose of naloxone s.c. The data suggest the possibility that dermorphin could affect gastrointestinal transit through an action on central and peripheral opiate receptors.

Animals↗

PubMed1984

Roles of mu, delta and kappa opioid receptors in spinal and supraspinal mediation of gastrointestinal transit effects and hot-plate analgesia in the mouse.

The opioid receptors involved in the mediation of thermal analgesia (55 degrees C hot-plate) and inhibition of gastrointestinal transit at the spinal and supraspinal levels were studied in unanesthetized mice. Five receptor-selective compounds were evaluated for effectiveness in eliciting analgesia and inhibiting transit after both i.c.v. and intrathecal administration; these included the proposed mu agonist, [D-Ala2, N-methyl-Phe4, Gly5-ol]enkephalin (DAGO), the proposed delta agonists, [D-Pen2, L-Pen5]enkephalin (DPLPE), [D-Pen2, D-Pen5]enkephalin (DPDPE) (conformationally constrained delta selective enkephalin analogs) and [D-Thr2, Thr6, Leu5]enkephalin (DTTLE), and the proposed kappa agonist, trans-3,4-dichloro-N-methyl-N-[2-(1-pyrolidinyl)-cyclohexyl]- benzeneacetamide methanesulfonate (U-50,488H), as well as the nonselective mu-acting agonist, morphine. All compounds were found to produce analgesia after i.c.v. administration; the rank order of potency by the i.c.v. route was DAGO greater than DTTLE greater than morphine greater than DPLPE greater than DPDPE greater than U-50,488H. The analgesic effectiveness of most of these agonists given i.c.v. was evident for up to 40 min, with only DTTLE and U-50,488H having briefer time courses. Similarly, all the compounds produced analgesic responses after intrathecal administration, with the rank order of potency by this route being DTTLE greater than morphine greater than DAGO greater than DPLPE greater than DPDPE greater than U-50,488H, and all compounds (except U-50,488H) had durations of action of up to 20 to 40 min. These agonists also inhibited gastrointestinal transit after intrathecal administration, with a rank order of potency of DAGO greater than DTTLE greater than DPLPE greater than morphine greater than DPDPE greater than U-50,488H.(ABSTRACT TRUNCATED AT 250 WORDS)

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

PubMed1997

Reference ranges for gastrointestinal transit of barium-impregnated polyethylene spheres in healthy cats.

Commercial barium-impregnated polyethylene spheres (BIPS) were administered to 12 healthy adult cats according to the manufacturer's instructions (30 small BIPS and 10 large BIPS to each cat) together with 60 g of a canned food. Radiographs were taken at hourly intervals until seven hours after feeding, and then at eight, 10, 12, 14, 17, 23 and 30 hours or until all the BIPS had left the stomach and at least 50 per cent had entered the colon. Six cats were sedated immediately after being fed the BIPS and six cats remained unsedated. For small BIPS (1.5 mm diameter), the gastric transit time (first exit of BIPS from the stomach) in the sedated cats had a median of 6 hours (range 3 to 8) and in the unsedated cats a median of 2.5 hours (range 2 to 6). Values for other transit times were not significantly different between the two groups, and the pooled data revealed a median 50 per cent gastric emptying time of 6.4 hours (range 2.5 to 10.9), a complete gastric emptying time of 12 hours (range 6 to 27), an orocaecal transit time (first appearance of BIPS in the colon) of 6.5 hours (range 4.0 to 12.0) and a 50 per cent orocaecal transit time of 8.8 hours (range 4.6 to 12.8). The gastrointestinal transit of large BIPS (5 mm diameter) was significantly correlated with the passage of small BIPS but, except for the complete gastric emptying time, was significantly slower.

Animals↗

PubMedDate not supplied

[Efficacy and tolerance of cinitapride on the disturbances of gastrointestinal transit].

In order to evaluate the efficacy and tolerance of cinitapride, 103 patients with gastrointestinal disorders were admitted to a randomized, parallel, double blind trial for treatment with cinitapride, metoclopramide or placebo. Cinitapride was significantly more effective than metoclopramide in restoring normal defecation rates in constipated patients after 7 and 14 days of treatment (p = 0.036 and p = 0.008) and significantly more effective than placebo in restoring normal consistency of compact stools after 7 and 14 days of treatment (p = 0.006 and p = 0.051). Cinitrapide also proved to be significantly more effective than metoclopramide in curing or improving post-prandial epigastric distention (p = 0.031), post-prandial epigastric fullness (p = 0.037) and abdominal pain (p = 0.002) after 7 and 14 days of treatment. After treatment with cinitapride, dyspeptic symptoms disappeared or improved in 56-82% of patients. The efficacy rates in controlling gastrointestinal transit disorders, according to the investigators, were 64% for cinitapride, 28% for metoclopramide (p = 0.004) and 39% for placebo (p = 0.031) and, according to the patients, 55% for cinitapride, 25% for metoclopramide (p = 0.014) and 39% for placebo, 44% of the patients treated with cinitapride, 51% of the patients treated with metoclopramide and 26% of the patients treated with placebo reported and adverse reaction, with statistically significant differences between metoclopramide and placebo (p = 0.031). The tolerance rates, according to the investigators, were 82% for cinitapride, 64% for metoclopramide and 94% for placebo (placebo vs. metoclopramide, p = 0.001) and, according to the patients, 72% for cinitapride, 51% for metoclopramide and 89% for placebo (placebo vs. metoclopramide, p = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2000

Possible involvement of 5-HT and 5-HT2 receptors in acceleration of gastrointestinal transit by escin Ib in mice.

We have reported previously that escin Ib accelerated gastrointestinal transit (GIT) in mice, and that its effect may be mediated by the release of endogenous prostaglandins (PGs) and nitric oxide (NO). In this study, the possible involvement of 5-HT and 5-HT receptors in the GIT acceleration of escin Ib was investigated in mice. The acceleration of GIT by escin Ib (25 or 50 mg/kg, p.o.) was attenuated by pretreatment with ritanserin (0.5-5 mg/kg, s.c., a 5-HT(2A/2C/2B) receptor antagonist), but not with MDL 72222 (1 and 5 mg/kg, s.c.) and metoclopramide (10 mg/kg, s.c.) (5-HT3 receptor antagonists) or tropisetron (1 and 10 mg/kg, s.c., a 5-HT(3/4) receptor antagonist). Furthermore, pretreatment with ketanserin (0.05-5 mg/kg, s.c.), haloperidol (1-5 mg/kg, s.c.) and spiperone (0.5-5 mg/kg, s.c.) (5-HT2A receptor antagonists), as well as a bolus of dl-p-chlorophenylalanine methyl ester (PCPA, 1000 mg/kg, p.o., 1, 6 or 24 h before administration of the sample) (an inhibitor of 5-HT synthesizing enzyme tryptophan hydroxylase) and reserpine (5 mg/kg, p.o.) (a 5-HT depletor), but not 6-hydroxydopamine (80 mg/kg, i.p., a dopamine depletor) or repeated PCPA (300 mg/kg x2, p.o., 72 and 48 h before administration of the sample), also attenuated the effects of escin Ib. It is postulated that escin Ib accelerates GIT, at least in part, by stimulating the synthesis of 5-HT to act through 5-HT2, possibly 5-HT2A receptors, which in turn causes the release of NO and PGs.

Animals↗

PubMed1998

[The effect of pretreatment with ranitidine on the pharmacokinetics and gastrointestinal transit of a sustained-release theophylline preparation].

A scintigraphic and pharmacokinetic study of the behavior of Bronchoretard forte (theophylline, CAS 58-55-9) was carried out in 8 healthy male volunteers to evaluate the sensitivity of the preparation to changes in gastric pH. The volunteers were pretreated with ranitidine (CAS 66357-35-5) (150 mg b.i.d.) or placebo for three days prior to and on the study day to reduce gastric acidity. The effect of the pretreatment with ranitidine on gastric pH was measured on the day before study begin and the mean pH was significantly increased compared to the placebo (ranitidine pH 2.2 +/- 2.4; placebo pH 1.6 +/- 2.0, p < 0.01 Wilcoxon Signed Rank test). All subjects were pretreated with theophylline for 3 days (500 mg b.i.d.) to achieve steady state. On the study day, the volunteers swallowed two theophylline sustained release capsules, radiolabelled by inclusion of indium-111 micronised Amberlite resin, and the gastrointestinal transit was followed continuously for 14 h using gamma scintigraphy with a further image at 24 h. Blood samples were taken from each subject throughout the study to determine the pharmacokinetic profile of theophylline in the sustained release formulation. No significant differences were found in the gastrointestinal transit of the labelled microparticulates between the data obtained from the group treated with ranitidine and that from the placebo group. Plasma theophylline concentration profiles were identical for the two treatments. These data indicate that the theophylline sustained release formulation is not sensitive to the effects of major changes in gastric H+ concentration.

Adult↗

PubMed1991

Effect of pretreatment with ranitidine on the pharmacokinetics and gastrointestinal transit of a sustained release theophylline preparation.

A scintigraphic and pharmacokinetic study of the behaviour of (Bronchoretard forte, CAS 58-55-9) was carried out in 8 healthy male volunteers to evaluate the sensitivity of the preparation to changes in gastric pH. Volunteers were pretreated with ranitidine (CAS 66357-35-5) (150 mg b.d.) or placebo for three days prior to and on the study day to reduce gastric acidity. The effect of the pretreatment with ranitidine on gastric pH was measured on the prestudy day and the mean pH was significantly reduced compared to the placebo (ranitidine pH 2.2 +/- 2.4; placebo pH 1.6 +/- 2.0, p less than 0.01 Wilcoxon Signed Rank test). All subjects were pretreated with theophylline for 3 days (500 mg b.d.) to achieve steady-state. On the study day the volunteers swallowed two theophylline sustained release capsules radiolabelled by inclusion of indium-111 micronised Amberlite resin and the gastrointestinal transit followed continuously for 14 h using gamma scintigraphy with a further image at 24 h. Blood samples were taken from each subject throughout the study to determine the pharmacokinetic profile of theophylline when presented in the sustained release formulation. No significant differences were found in the gastrointestinal transit of the labelled microparticulates between the data obtained from the group when treated with ranitidine or placebo. Plasma theophylline concentration profiles were identical for the two treatments. These data indicate that the theophylline sustained release formulation is not sensitive to the effects of major changes in gastric H+ concentration.

Adult↗

PubMedDate not supplied

The effect of chilli and its pungent ingredient capsaicin on gastrointestinal transit in the rat.

The effect of chilli powder and its pungent ingredient capsaicin on gastrointestinal transit in the rat was studied. Fasted unanaesthetized male Sprague-Dawley rats (n = 144) received by gavage a test meal containing charcoal and cellulose in water or capsaicin solvent plus 51Cr as a radioactive marker. Either 100 or 200 mg of chilli powder (containing 0.13 and 0.26 mg of capsaicin, respectively) or 0.5 or 1 mg of capsaicin were added, the final volume of each meal being 1.5 mL. At 10 and 20 min, animals were killed and the amount of isotope that had left the stomach was measured, together with the distance the charcoal column had travelled along the small intestine. Compared to controls, animals given chilli powder emptied less of their gastric content at 10 and 20 min, an effect partly reproduced by capsaicin. However overall gastric-small intestinal transit was unaffected by chilli powder or capsaicin. Another 12 male Sprague-Dawley rats received, under light ether anaesthesia, on six occasions at 1-2 week intervals, the same six test meals as used in the previous experiment except that charcoal was not used. Total gut transit as measured by the amount of radioactive marker excreted in the stools at 18 and 24 h was unaffected by the use of chilli or capsaicin.

Animals↗

PubMed2001

Effects of an alpha(2)-adrenergic agonist on gastrointestinal transit, colonic motility, and sensation in humans.

To characterize alpha(2)-adrenergic control of motor and sensory functions of gastrointestinal tract and colon, we studied dose-related effects of clonidine (placebo or up to 0.3 mg po) by random assignment in 55 healthy humans. Gastrointestinal transit was measured in all subjects; in 35, we assessed colonic compliance, tone, and sensations of gas and pain during phasic distensions. Clonidine did not significantly alter gastrointestinal or colonic transit, but it increased colonic compliance and reduced fasting tone without altering colonic response to a meal. Clonidine significantly reduced aggregate sensation to distensions overall and had significant linear dose-related sensory effects at 8- and 24-mmHg distensions. Effect on pain (including dose-response relationship) was due to 0.3-mg dose for distensions at 24 mmHg. We confirmed that clonidine relaxes fasting colonic tone and reduces sensation of pain. In this study, gut transit was not altered by clonidine, and novel dose-response characteristics and clonidine's effect on gas sensation are provided. Doses as low as 0.05 mg may be effective and potentially useful in reducing colonic tone and gas sensation.

Adrenergic alpha-Agonists↗

PubMed1989

Stress effects on gastrointestinal transit in the rat.

Previous investigations of stress effects on gastric emptying, orocaecal, and colonic transit in rats have produced conflicting results. Here one type of stressor, a 'passive avoidance' situation, was used to investigate its effects on gastric emptying, orocaecal and colonic transit. After the rats had been trained to eat a standard amount of semisolid food, gastric emptying was determined (n = 12) by the food remaining in the stomach after various periods of rest, or stress exposure. Orocaecal transit (n = 14) was determined by breath hydrogen measurements after the food had been labelled with 1 g lactose. Colonic transit (n = 18) was measured as the arrival time of coloured faeces after infusion of a carmine red solution into the caecum through a chronically implanted catheter. The stressor had differential effects on transit through the stomach, small bowel and colon: gastric emptying was delayed (p less than 0.05) after stress (t1/2 = 2.66 h after stress, 1.97 h at rest). Orocaecal transit was accelerated (p less than 0.05) after stress; transit time decreased from 124.3 min at rest to 86.2 min after stress. Colonic transit was accelerated (p less than 0.01) under stress, from 15.5 h to 1.29 h. It is concluded that gastrointestinal transit in different parts of the gastrointestinal tract is differently affected by central nervous stimuli.

Animals↗

PubMed1989

Differential development of acute tolerance to analgesia, respiratory depression, gastrointestinal transit and hormone release in a morphine infusion model.

To determine whether the differences in development of acute tolerance to several morphine actions correlate with the mu receptor subtype mediating them, we have examined the appearance of acute tolerance to analgesia, respiratory depression, gastrointestinal transit, and hormone release in an intravenous morphine infusion model. Analgesia, a naloxonazine-sensitive mu1 action, peaked at 2 hr after initiation of the infusions. The log dose-response relationship of the infusion rate to peak tailflick latency was linear from 10 to 50 micrograms/kg/min. By 8 hr, the tailflick latencies declined nearly to baseline levels, implying the rapid development of tolerance. Tolerance to morphine-induced prolactin release, another mu1 action, also developed rapidly over 8 hr. In contrast two mu2 actions, respiratory depression measured with arterial blood gas, determinations and gastrointestinal transit, showed no significant tolerance over a similar 8 hr infusion. We also observed no tolerance to morphine-induced growth hormone release, a non-mu1 action, over the same period. Thus, these results demonstrate that mu1 actions develop tolerance in an infusion model far more rapidly than a number of naloxonazine-insensitive (non-mu1) ones and may help explain differences in the rate of tolerance development to morphine actions.

Analgesia↗

PubMed2004

Hydrolysis of casein accelerates gastrointestinal transit via reduction of opioid receptor agonists released from casein in rats.

BACKGROUND: Protein hydrolysate accelerates gastrointestinal transit (GIT) and feeding advancement in preterm infants compared to native protein. In rat pups, opioid receptor agonists released from casein during digestion such as beta-casomorphins slow down GIT. We hypothesized that hydrolysis of casein reduces the opioid activity released during digestion thereby accelerating GIT compared to native casein. OBJECTIVE: The aim of the present study was to investigate whether casein hydrolysate accelerates GIT compared to native casein and whether pretreatment with naloxone, an opioid receptor blocker, abolishes this difference in rat pups. METHODS: In a randomized controlled trial following a 2 x 2 factorial design, 216 female Wistar rat pups were fed with pellets based on hydrolyzed or native casein. After pretreatment with naloxone or normal saline, carmine red was administered by oro-gastric gavage as a tracer for GIT velocity measurement. Four hours later the animals were sacrificed, their intestine was removed and the length of the colon from the cecocolonic junction to the anus was measured. GIT was recorded as percentage of the total colonic length (percentage of colonic transit) passed by carmine red. Data were given as mean +/- SD. RESULTS: GIT was significantly higher with hydrolyzed casein compared to native casein formula (77.4 +/- 17 and 51.2 +/- 20%), but there was no difference after naloxone pretreatment (77.1 +/- 16 and 76.5 +/- 17%). DISCUSSION: The present data suggest that hydrolysis of casein accelerates GIT via reduction of opioid activity released during digestion. Further studies are required to investigate to which extent these rat pub data apply to preterm infants.

Animals↗

PubMed2002

Gastrointestinal transit in an animal model of human diabetes type 2: relationship to gut neuroendocrine peptide contents.

Gastrointestinal transit (GIT) was determined in obese diabetic mice (ob/ob, Umeå/Bom). Blood glucose level, and insulin concentration in the serum and pancreas extracts as well as neuroendocrine peptide contents were measured in several segments of the gut. GIT was significantly slower in the obese diabetic mice, but was not correlated with the blood glucose level, serum insulin, or pancreatic insulin content. GIT was correlated with duodenal secretin content and colonic vasoactive intestinal peptide (VIP) content, but not with the content of other neuroendocrine peptides in different segments investigated. The antral gastrin content in obese diabetic mice was significantly higher than in controls. The concentration of secretin in obese diabetic mice was higher than in controls. Whereas the contents of peptide YY (PYY) and somatostatin were higher in obese diabetic mice, the contents of substance P and VIP were lower. The increased content of duodenal secretin and decreased content of colonic VIP may be among the factors that cause slow GIT in obese diabetic mice. The changes in the colonic contents of PYY, VIP and somatostatin may cause low intestinal secretion and, together with slow GIT, give rise to constipation, which is a common symptom in diabetes.

Animals↗

PubMed1990

Effects of cisapride on gastrointestinal transit in healthy humans.

It was the aim of this study to assess the effects of cisapride on gastrointestinal transit of solids in healthy humans. Twelve men received cisapride 10 mg or placebo orally four times a day in random, double-blind, crossover fashion. Transit measurements were performed with a new gamma camera technique. Cisapride reduced mean gastric emptying time of 99mTc-labeled cellulose fiber [0.77 (0.69-1.12) hr [median (range)] vs 0.98 (0.63-1.95) hr; P less than 0.05] and 1- to 2-mm 111In-labeled plastic particles [1.08 (0.50-1.42) hr vs 1.69 (0.59-3.03) hr; P less than 0.01]. Cisapride also decreased mean small intestinal transit time of cellulose fiber [2.11 (0.80-5.08) hr vs 2.82 (0.78-7.12) hr; P less than 0.05] and plastic particles [2.06 (1.13-5.13) hr vs 2.64 (1.18-7.04) hr; P less than 0.05]. However, cisapride increased mean large intestinal transit time of plastic particles [31 (13-75) hr vs 23 (12-36) hr; P less than 0.05]. In conclusion, oral cisapride 10 mg four times a day accelerates gastric emptying and small intestinal transit whereas this dose of cisapride seems to delay large intestinal transit of solids in healthy humans.

Adult↗

PubMed1979

A new method for the determination of gastrointestinal transit times.

A new method for the determination of the gastrointestinal transit time (TT) is described. The normal range of the TT was 40--95 h in 58 normal subjects. No age or sex variation of the TT was disclosed. In 25 out-patients with the irritable bowel syndrome the TT was determined before and after 3 weeks' treatment with Vi-Siblin. Of these patients, 20% initially showed a prolonged TT; this decreased during treatment with Vi-Siblin. In the patients with normal TT, this remained unchanged during the treatment. Our study suggests that patients with long TT, long intervals between bowel movements, and frequent attacks of colicky abdominal pain may derive benefit from a plant fibre supplement to their diet. The method for the determination of the TT described is well suited to out-patient studies--also in large populations--since it is relatively easy to perform, stool collection is unnecessary, and the method shows good reproducibility.

Adult↗

PubMed1999

Effects of oleanolic acid glycosides on gastrointestinal transit and ileus in mice.

The effects of various oleanolic acid glycosides obtained from medicinal herbs on gastrointestinal transit (GIT) and ileus were investigated in fasted mice. Ileus was induced by the peritoneal-irritation or by the laparotomy with manipulation. One hour after the oral administration, three oleanolic acid 3-O-monodesmosides (oleanolic acid 3-O-glucuronide (3, 50 mg/kg), momordin Ic (4, 25 and 50 mg/kg), and momordin I (6, 25 mg/kg)) significantly accelerated GIT, but two oleanolic acid 3-O-monodesmosides (28-deglucosyl-chikusetsusaponins IV (8) and V (10)), oleanolic acid 3,28-O-bisdesmosides (momordin IIc (5), chikusetsusaponins IV (7) and V (9)), and their common aglycon (oleanolic acid (1)) (50 mg/kg) showed no significant effect. On the other hand, oleanolic acid 28-O-monodesmoside (compound O (2, 50 mg/kg)) significantly inhibited GIT. 4 (5-25 mg/kg) and 6 (12.5 and 25 mg/kg) also significantly prevented the inhibition of GIT induced by the peritoneal injection of acetic acid. 2 and 9 (50 mg/kg) significantly potentiated the inhibition of GIT, whereas 1, 3, 5, 7, 8, and 10 (50 mg/kg) showed no significant effect. 3, 4, 6, and 10 (50 mg/kg) significantly prevented the inhibition of GIT induced by laparotomy with manipulation, while 1, 2, 5, 7, 8, and 9 (50 mg/kg) showed no significant effect. These results indicate that the 3-O-glycoside moiety seems to be essential to show the GIT accelerating activity, and the 28-O-glucoside moiety reduce the activity. The accelerations of GIT by 3, 4, and 6 were completely abolished by the pretreatment with streptozotocin (100 mg/kg, i.v.), but not by the pretreatment with capsaicin (75 mg/kg in total, s.c.). These results suggest that sympathetic nervous system, but not capsaicin-sensitive sensory nerves, be involved in the enhancements of GIT by 3, 4, and 6. It is worthy to study their therapeutical effect in the prevention of the inhibition of GIT, including ileus, in clinic.

Animals↗