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PubMed2001

Gastric electrical activity and gastric emptying in preterm newborns fed standard and hydrolysate formulas.

BACKGROUND: Because infant formulas containing hydrolyzed cow milk protein are used to reduce feeding intolerance and to improve gastric emptying, the effect on gastrointestinal motility of a hydrolysate formula was compared with that of a standard preterm formula. METHODS: Thirty-six preterm newborns with a gestational age of 32.2 +/- 2.3 weeks were assigned randomly to standard formula or hydrolyzed formula. Cutaneous electrogastrography and ultrasound examination of gastric emptying were performed simultaneously to evaluate gastrointestinal motility before and after the test meal. All recording sessions were performed 1 week after infants had reached full enteral feeding. RESULTS: No significant difference in gastrointestinal symptoms was noted in the newborns fed the different formulas. In particular, regurgitation and vomiting were observed in 78% versus 64% of preterm newborns after standard and hydrolyzed formula, respectively (Fisher exact test, not significant). No differences were found in terms of gastric electrical activity and gastric emptying time between the two groups. CONCLUSIONS: It seems unnecessary to use hydrolysate formulas to improve motility in preterm infants.

Electromyography↗
PubMed2006

Glial-derived neurotrophic factor modulates enteric neuronal survival and proliferation through neuropeptide Y.

BACKGROUND & AIMS: Glial-derived neurotrophic factor (GDNF) promotes the survival and proliferation of enteric neurons. Neuropeptide Y (NPY) is an important peptide regulating gastrointestinal motility. The role of NPY on the survival and proliferation of enteric neurons is not known. We examined the effects of GDNF on the expression and release of NPY from enteric neurons and the role of NPY in promoting enteric neuronal proliferation and survival. METHODS: Studies were performed in primary enteric neuronal cultures and NPY knockout mice (NPY(-/-)). GDNF-induced expression of NPY was assessed by reverse-transcription polymerase chain reaction (RT-PCR), immunocytochemistry, and enzyme-linked immunosorbent assay. Using NPY-siRNA and NPY-Y1 receptor antagonist, we examined the role of NPY in mediating the survival and proliferation effects of GDNF. Gastrointestinal motility was assessed by measuring gastric emptying, intestinal transit, and isometric muscle recording from intestinal muscle strips. RESULTS: GDNF induced a significant increase in NPY messenger RNA and protein expression in primary enteric neurons and the release of NPY into the culture medium. NPY (1 mumol/L) significantly increased proliferation of neurons and reduced apoptosis. In the presence of NPY-siRNA and NPY-Y1 receptor antagonist or in enteric neurons cultured from NPY(-/-) mice, GDNF-mediated neuronal proliferation and survival was reduced. NPY increased the phosphorylation of Akt, a downstream target of the PI-3-kinase pathway. In NPY(-/-) mice, there were significantly fewer nNOS-containing enteric neurons compared with wild-type (WT) mice. NPY(-/-) mice had accelerated gastric emptying and delayed intestinal transit compared with WT mice. CONCLUSIONS: We demonstrate that NPY acts as an autocrine neurotrophic factor for enteric neurons.

Animals↗
PubMed2000

Lack of responses to a beta3-adrenergic agonist in lipoatrophic A-ZIP/F-1 mice.

Stimulation of beta3-adrenergic receptors increases metabolic rate via lipolysis in white adipose tissue (WAT) and thermogenesis in brown adipose tissue (BAT). Other acute effects include decreased gastrointestinal motility and food intake and increased insulin secretion. Chronic treatment with a beta3 agonist ameliorates diabetes and obesity in rodents. We studied the effects of beta3 stimulation in A-ZIP/F-1 mice, which have virtually no WAT, a reduced amount of BAT, severe insulin resistance, and diabetes. In contrast with wild-type mice, treatment of A-ZIP/F-1 mice with CL316243, a beta3-adrenergic agonist, did not increase O2 consumption. A single dose of CL316243 produced a 2-fold increase in serum free fatty acids, a 53-fold increase in insulin, and a 2.4-fold decrease in glucose levels in wild-type mice but no change in A-ZIP/F-1 animals. The A-ZIP/F-1 mice also did not show reduced gastrointestinal motility or 24-h food intake during beta3 stimulation. Chronic administration of CL316243 to the A-ZIP/F-1 mice did not improve their thermogenesis, hyperglycemia, or hyperinsulinemia. Thus, all of the beta3 effects studied were absent in the lipoatrophic A-ZIP/F-1 mice, including the effects on nonadipose tissues. From these results, we suggest that all of the effects of beta3 agonists are initiated at the adipocyte with the nonadipose effects being secondary events presumably mediated by signals from adipose tissue.

Adipose Tissue↗
PubMed2003

Smooth muscle contraction induced by Indigofera dendroides leaf extracts may involve calcium mobilization via potential sensitive channels.

The contractile effects of the aqueous extract of the leaves of Indigofera dendroides (ID) were studied on the gastrointestinal motility in mice and isolated smooth muscle preparations obtained from rats and guinea pigs. The contractile effects of 10(-6) M acetylcholine, 80 mM KCl and 1.6 mg/ml ID were measured on the rat ileal smooth muscle exposed to calcium-free buffer or physiological solution, to determine the calcium pools mobilized by extract for activation of contraction. Acute toxicity test (LD(50)) was also carried out in mice. The result showed that ID (0.05-3.2 mg/ml) produced a concentration-dependent contraction of the guinea pig and rat ileum. These responses were not blocked by mepyramine (2.49 x 10(-9) M), verapamil (8.14 x 10(-9) M), or pirenzepine (4.7 x 10(-7) M), but were blocked completely by atropine (2.92 x 10(-9) M). A significant increase in propulsion of gastrointestinal motility was observed. Acetylcholine, KCl and ID produced contractions in Ca(2+) free media. The phasic components of the contractile responses to Ach as well as the tonic component of K(+) and ID-induced contractions were relatively resistant to short periods of calcium-free exposure. Ach, K(+) and ID still caused contractions in the presence of verapamil. The data revealed that ID-induced contractions were not mediated by histaminergic receptors, calcium channels, M1 muscarinic receptors. It also suggests that Ach mobilize Ca from some tightly bound or intracellular pool, whereas high K(+) and ID may mobilize Ca from some superficial or loosely-bound pool.

Acetylcholine↗
PubMed2006

[Effects of acute hypobaric hypoxia on gastric emptying and intestinal propulsion: experiment with rats].

OBJECTIVE: To investigate the impact of acute hypobaric hypoxia on the gastrointestinal motility. METHODS: Eighty Wistar rats were randomly divided into 4 equal groups to be fed with (99)Tc(m)-labeled test food: ground level control group, put in the hypobaric chamber for 30 minutes; 3000 m simulated altitude group, exposed to the environment of simulated altitude of 3000 m for 30 minutes; 5000 m simulated altitude group, exposed to the environment of simulated altitude of 5000 m for 30 minutes; and mosapride + 5000 m simulated altitude group, fed with mosapride 2 mg/kg by perfusing stomach and fed with isotope-labeled test food 30 minutes later, and then exposed to 5000 m simulated altitude for 30 minutes. By the end of experiment the rats were killed, their stomachs were taken out to calculate the gastric emptying rate. Their intestine from pylorus to ileocecum was taken out to measure the intestinal propulsion function by using charcoal particle method. At the beginning and at the end of experiment abdominal arterial blood samples were collected to detect the plasma motilin and nitric oxide (NO) concentrations. RESULTS: The gastric emptying rate of the 5000 m simulated altitude group was 41% +/- 10%, significantly lower than that of the ground level group (62% +/- 12%, P < 0.01), and the charcoal transit rate of the 5000 m simulated altitude group was 37% +/- 8%, significantly lower than that of the ground level group (61% +/- 13%, P < 0.01). The gastric emptying rate and intestine propulsion rate of the 3000 m simulated altitude group were not significantly different from those of the ground level group. The gastric emptying rate of the mosapride + 5000 m simulated altitude group was 55% +/- 12%, significantly higher than that of the 5000 m simulated altitude group (P < 0.05), however, the intestine propulsion rate of the mosapride + 5000 m simulated altitude group was not significantly different from that of the 5000 m simulated altitude group (P > 0.05). The plasma motilin level of the 5000 m simulated altitude group was 88 pg/ml +/- 19 pg/ml, significantly lower than that of the ground level group (123 pg/ml +/- 28 pg/ml, P < 0.01), in contrast, the plasma NO level of the 5000 m simulated altitude group was 106 micromol/L +/- 24 micromol/L, significantly higher than that of the ground level group (80 micromol/L +/- 18 micromol/L, P < 0.01). CONCLUSION: Acute exposure to hypobaric hypoxia at the height of 5000 m inhibits the gastric emptying and intestinal propulsion. Mosapride may alleviate the inhibitory effect of hypobaric hypoxia on gastric emptying. Decrease of plasma motilin and elevation of NO level may be the main mechanism of inhibition of gastrointestinal motility by hypobaric hypoxia.

Animals↗
PubMed2001

Cannabinoids and the gastrointestinal tract.

The enteric nervous system of several species, including the mouse, rat, guinea pig and humans, contains cannabinoid CB1 receptors that depress gastrointestinal motility, mainly by inhibiting ongoing contractile transmitter release. Signs of this depressant effect are, in the whole organism, delayed gastric emptying and inhibition of the transit of non-absorbable markers through the small intestine and, in isolated strips of ileal tissue, inhibition of evoked acetylcholine release, peristalsis, and cholinergic and non-adrenergic non-cholinergic (NANC) contractions of longitudinal or circular smooth muscle. These are contractions evoked electrically or by agents that are thought to stimulate contractile transmitter release either in tissue taken from morphine pretreated animals (naloxone) or in unpretreated tissue (gamma-aminobutyric acid and 5-hydroxytryptamine). The inhibitory effects of cannabinoid receptor agonists on gastric emptying and intestinal transit are mediated to some extent by CB1 receptors in the brain as well as by enteric CB1 receptors. Gastric acid secretion is also inhibited in response to CB1 receptor activation, although the detailed underlying mechanism has yet to be elucidated. Cannabinoid receptor agonists delay gastric emptying in humans as well as in rodents and probably also inhibit human gastric acid secretion. Cannabinoid pretreatment induces tolerance to the inhibitory effects of cannabinoid receptor agonists on gastrointestinal motility. Findings that the CB1 selective antagonist/inverse agonist SR141716A produces in vivo and in vitro signs of increased motility of rodent small intestine probably reflect the presence in the enteric nervous system of a population of CB1 receptors that are precoupled to their effector mechanisms. SR141716A has been reported not to behave in this manner in the myenteric plexus-longitudinal muscle preparation (MPLM) of human ileum unless this has first been rendered cannabinoid tolerant. Nor has it been found to induce "withdrawal" contractions in cannabinoid tolerant guinea pig ileal MPLM. Further research is required to investigate the role both of endogenous cannabinoid receptor agonists and of non-CB1 cannabinoid receptors in the gastrointestinal tract. The extent to which the effects on gastrointestinal function of cannabinoid receptor agonists or antagonists/inverse agonists can be exploited therapeutically has yet to be investigated as has the extent to which these drugs can provoke unwanted effects in the gastrointestinal tract when used for other therapeutic purposes.

Acetylcholine↗
PubMed1995

The use of poly R-478 as a marker to determine gastric emptying and intestinal propulsive motility in suckling rats.

During our studies on gastrointestinal motility in suckling rats using 51Cr or 51Cr-EDTA as markers, we noticed that these markers--in contrast to studies in adult rats--"adhered" to the gastrointestinal wall of sucklings. We therefore decided to test the use of another non-absorbable marker Poly R-478 (an acetylated anthrapyridone chromophore linked to an polyamino-ethylene-sodium ethylene sulfonate copolymer backbone developed by the Dynapol Corporation (Palo Alto, CA). This new method has appeared to be useful.

Animals↗
PubMed2006

A deficiency of gastric interstitial cells of Cajal accompanied by decreased expression of neuronal nitric oxide synthase and substance P in patients with type 2 diabetes mellitus.

BACKGROUND: Gastrointestinal motility is impaired in patients with diabetes mellitus (DM). Interstitial cells of Cajal (ICC) in the gastrointestinal tract play a central role in gastrointestinal motility. The present study examined whether ICC density, or expression of neuronal nitric oxide synthase (nNOS)- and substance P (SP)-containing nerves in the gastric antrum, were altered in patients with type 2 DM. METHODS: Paraffin-embedded gastric specimens from 51 controls and 36 male DM patients with gastric cancer were used for immunohistochemistry. Serial sections were stained with Kit and mast cell tryptase-specific antibodies. Fresh-frozen gastric specimens from patients with gastric cancer were used for immunofluorescence. The specimens were stained with antibodies to Kit, nNOS, and SP, and levels of expression of these three markers were compared between controls and DM patients. RESULTS: ICC density in the inner circular muscle layer, but not in the myenteric plexus, was lower in patients with severe DM than in controls in paraffin-embedded specimens. In addition, decreased expression of nNOS and SP accompanied by reduced ICC density was observed in frozen specimens from patients with DM. CONCLUSIONS: These results suggest that lower gastric ICC, nNOS, and SP densities in patients with DM may be associated with the pathogenesis of diabetic gastroparesis.

Biomarkers↗
PubMed2006

Little or no ability of obestatin to interact with ghrelin or modify motility in the rat gastrointestinal tract.

BACKGROUND AND PURPOSE: Obestatin, encoded by the ghrelin gene may inhibit gastrointestinal (GI) motility. This activity was re-investigated. EXPERIMENTAL APPROACH: Rat GI motility was studied in vitro (jejunum contractility and cholinergically-mediated contractions of forestomach evoked by electrical field stimulation; EFS) and in vivo (gastric emptying and intestinal myoelectrical activity). Ghrelin receptor function was studied using a GTPgammaS assay and transfected cells. KEY RESULTS: Contractions of the jejunum or forestomach were unaffected by obestatin 100 nM or 0.01-1000 nM, respectively (P>0.05 each; n=4-18). Obestatin (0.1-1 nM) reduced the ability of ghrelin 1 microM to facilitate EFS-evoked contractions of the stomach (increases were 42.7+/-7.8% and 21.2+/-5.0 % in the absence and presence of obestatin 1 nM; P<0.05; n=12); higher concentrations (10-1000 nM) tended to reduce the response to ghrelin but changes were not statistically significant. Similar concentrations of obestatin did not significantly reduce a facilitation of contractions caused by the 5-HT(4) receptor agonist prucalopride, although an inhibitory trend occurred at the higher concentrations (increases were 69.3+/-14.0% and 42.6+/-8.7% in the absence and presence of 1000 nM obestatin; n=10). Obestatin (up to 10 microM) did not modulate recombinant ghrelin receptor function. Ghrelin increased gastric emptying and reduced MMC cycle time; obestatin (1000 and 30,000 pmol kg(-1) min(-1)) had no effects. Obestatin (2500 pmol kg(-1) min(-1), starting 10 min before ghrelin) did not prevent the ability of ghrelin (500 pmol kg(-1) min(-1)) to shorten MMC cycle time. CONCLUSIONS AND IMPLICATIONS: Obestatin has little ability to modulate rat GI motility.

Animals↗
PubMed2003

Prevention and treatment of gastrointestinal complications in patients on mechanical ventilation.

There exists a complex, dynamic interaction between mechanical ventilation and the splanchnic vasculature that contributes to a myriad of gastrointestinal tract complications that arise during critical illness. Positive pressure-induced splanchnic hypoperfusion appears to play a pivotal role in the pathogenesis of these complications, the most prevalent of which are stress-related mucosal damage, gastrointestinal hypomotility and diarrhea. Furthermore, characteristics of the splanchnic vasculature make the gastrointestinal tract vulnerable to adverse effects related to positive pressure ventilation. While most of these complications seen in mechanically ventilated patients are reflections of altered gastrointestinal physiology, some may be attributed to medical interventions instituted to treat critical illness. Since maintenance of normal hemodynamics cannot always be achieved, pharmacologic prophylactic therapy has become a mainstay in the prevention of gastrointestinal complications in the intensive care unit. Improved understanding of the systemic effects of mechanical ventilation and greater application of lung-protective ventilatory strategies may potentially minimize positive pressure-induced reductions in splanchnic perfusion, systemic cytokine release and, consequently, reduce the incidence of gastrointestinal complications associated with mechanical ventilation. Herein, we discuss the pathophysiology of gastrointestinal complications associated with mechanical ventilation, summarize the most prevalent complications and focus on preventive strategies and available treatment options for these complications. The most common causes of gastrointestinal hemorrhage in mechanically ventilated patients are bleeding from stress-related mucosal damage and erosive esophagitis. In general, histamine H(2) receptor antagonists and proton pump inhibitors prevent stress-related mucosal disease by raising the gastric fluid pH. Proton pump inhibitors tend to provide more consistent pH control than histamine H(2) receptor antagonists. There is no consensus on the drug of choice for stress ulcer prophylaxis with several meta-analyses providing conflicting results on the superiority of any medication. Prevention of erosive esophagitis include careful use of nasogastric tubes and institution of strategies that improve gastric emptying. Many mechanically ventilated patients have gastrointestinal hypomotility and diarrhea. Treatment options for gastrointestinal motility are limited, thus, preventive measures such as correction of electrolyte abnormalities and avoidance of medications that impair gastrointestinal motility are crucial. Treatment of diarrhea depends on the underlying cause. When associated with Clostridium difficile infection antibacterial therapy should be discontinued, if possible, and treatment with oral metronidazole should be initiated.More studies are warranted to better understand the systemic effects of mechanical ventilation on the gastrointestinal tract and to investigate the impact of lung protective ventilatory strategies on gastrointestinal complications.

Gastrointestinal Diseases↗
PubMed1987

The effect of two alpha 2-adrenoreceptor agonists and an antagonist on gastric emptying and mouth to caecum transit time in humans.

Experiments were performed to investigate the effect of two alpha 2-adrenoreceptor agonists, clonidine and lidamidine, and a specific alpha 2-adrenoreceptor antagonist, idazoxan, on gastric emptying and mouth to caecum transit time (MCTT) of a radiolabelled meal in 27 healthy male subjects. Lidamidine (20 mg p.o.) and clonidine (0.3 mg p.o.), given alone had no significant effect on gastric emptying or MCTT suggesting that the anti-diarrhoeal action of clonidine and lidamidine are unlikely to be explained by a slowing of small intestinal transit. Idazoxan (20 mg p.o.) reversed the effect of clonidine in 10 subjects, who showed a delay in MCTT after taking clonidine, but did not alter MCTT under basal conditions. These results suggest that although the sympathetic nervous system can influence upper gastrointestinal motility by an action on alpha 2-adrenoreceptors, this action does not exert a tonic influence on upper gastrointestinal motility under basal conditions.

Adolescent↗
PubMed1995

Pertussis and cholera toxins modulate kappa-opioid receptor agonists-induced hypothermia and gut inhibition.

In mice pretreated intracerebroventricularly (i.c.v.) with either saline (10 microliters/mouse), pertussis (1 microgram/mouse) or cholera (2.5 micrograms/mouse) toxins, effect of kappa-opioid receptor agonists on the colonic temperature and charcoal meal transit time were assessed. The kappa-opioid receptor agonist, trans-(+)-3,4-dichloro-N-methyl-[2-(1- pyrrolidinyl)cyclohexyl]-benzeneacetamide methane sulfonate hydrate (U-50488H, 50, 100 and 200 micrograms/mouse, i.c.v.) produced dose dependent hypothermia. Pertussis toxin pretreatment (72 and/or 144 h before) antagonized (P < 0.05) the hypothermic effect of U-50488H (100 micrograms/mouse) and (+)-trans-N-methyl-N-[2-(1- pyrrolidinyl)cyclohexyl[benz[b]-thio-phene-4-acetamide (PD 117302, 30 micrograms/mouse). In contrast, cholera toxin pretreatment (48 and/or 96 h before) did not antagonize the hypothermic effect of the kappa-opioid receptor agonists. Moreover, both i.c.v. and intrathecal (i.t.) administration of kappa-opioid receptor agonists, U-50488H, }[5R-(5 alpha,7 alpha,8 beta)]-(+/-)-N-methyl-N-[7-(1- pyrrolidinyl)-1-oxaspiro[4,5]dec-8-yl]-benzeneacetamide¿ (U-69593) and PD 117302, produced dose dependent inhibition of the charcoal meal transit. Cholera toxin pretreatment (48 and 96 h before) augmented (P < 0.05) the antitransit effect of i.c.v. administered U-50488H (100 micrograms/mouse), U-69593 (100 micrograms/mouse) and PD 117302 (50 micrograms/mouse). However, pertussis toxin pretreatment did not affect the gastrointestinal inhibitory effect of the kappa-opioid receptor agonists. The present results extend our previous results on the effect of kappa-selective agonists on gastrointestinal motility and indicate, like the prototype opiate agonist morphine, kappa-opioid receptor agonists are effective in inhibiting the gastrointestinal motility when administered either by intrathecal or intracerebroventricular routes.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1995

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

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

Acute Disease↗
PubMed2006

Gastroesophageal reflux disease, colic and constipation in infants with food allergy.

PURPOSE OF REVIEW: This review assesses the role of food allergy in the pathophysiology of gastroesophageal reflux disease, colic and constipation in infancy. RECENT FINDINGS: Frequent regurgitation, persistent crying and constipation are common clinical problems in infancy. A subgroup of infants with these conditions may respond to hypoallergenic diets, but only few randomized clinical trials have been conducted. Skin prick testing and food-specific antibody levels are usually not elevated in these infants, whereas atopy patch testing may diagnostic. The mechanisms by which cow's milk and other food allergens induce gastrointestinal motility disorders are not understood. Apart from cell-mediated reactions, non-immunological effects of food constituents on gastrointestinal motility and gut microbiota may be involved in the pathogenesis. In the absence of reliable diagnostic tests, dietary elimination and re-challenge are usually required to confirm food allergy. A trial of amino acid-based formula or an oligoantigenic maternal elimination diet may be indicated in infants who have failed conventional medical treatment. SUMMARY: Food allergy may contribute to gastroesophageal reflux disease, colic or constipation in infancy. Infants with these conditions often respond to hypoallergenic formula or a maternal elimination diet. Further research is needed to define the mechanisms and clinical markers of gastrointestinal food allergy in infancy.

Colic↗
PubMed1986

Electrical activity of the stomach: clinical implications.

Disorders of gastrointestinal motility are increasingly being recognized with the aid of such innovative techniques as gastrointestinal manometry and radioscintigraphy. Applications of these techniques have expanded and refined our present understanding of the gut motility both in health and in disease. Recent studies have shown that disturbances of motility can be limited to a specific segment of the gut such as the stomach or can affect the entire gastrointestinal tract. Because gastrointestinal motility is controlled by electrical activity, increasing efforts are being made to characterize and quantify the underlying electrical disturbances in various disorders of gastrointestinal motility. In this article, we review the electrical basis of gastric motility and the clinical implications of gastric dysrhythmia.

Adult↗
PubMed2003

Antidiarrheal activity of the methanol extract of Ludwigia hyssopifolia Linn.

Dried whole plant parts of Ludwigia hyssopifolia were subjected to successive cold extraction with n-hexane, ethylacetate and methanol. The methanol extract (LHM), obtained as 1% yield, showed significant antidiarrheal property by reducing diarrheal episodes in castor oil and serotonin induced diarrhea in laboratory mice at a dose of higher than 100 mg/kg body weight as compared to standard drug loperamide given at a dose of 66.67 microg/kg body weight. The percent reduction in diarrheal episode by 56.32 and 89.66 after castor oil challenge and 59.09 and 86.36 in serotonin induced diarrhea was observed at doses of 200 mg/kg and 400 mg/kg body weight of the extract respectively. The extract LHM was also found to reduce the gastrointestinal motility by 53.8% at a dose of 100 mg/kg body weight as compared to control, while no remarkable inhibition of gastrointestinal motility was seen at a dose of 50 mg/kg body weight of the extract.

Journal Article↗
PubMed1988

Evidence for the involvement of corticotropin-releasing factor in the gastrointestinal disturbances induced by acoustic and cold stress in mice.

The influence of acoustic (AS) and cold (CS) stress on gastric emptying and intestinal transit were evaluated in mice using a radiolabelled 51chromium test meal. AS was produced by playing music through loudspeakers (less than 86 dB) in a confined box at room temperature (20 degrees C) and CS was obtained by exposure to 10 degrees C. Twenty minutes exposure to AS or CS caused a significant (P less than 0.05) increase in gastric emptying in mice. Intracerebroventricular (i.c.v.) administration of 150 ng of rat corticotropin-releasing factor (rCRF), 30 min before the test meal, also increased gastric emptying but neither intraperitoneal (i.p.) administration of rCRF at the same dosage nor corticosterone (300 ng) and ACTH (375 microU) were able to induce significant changes in gastric emptying. The increase in gastric emptying induced by AS and CS and by i.c.v. injection of rCRF were blocked by previous i.p. administration of an antiserum against rCRF. These findings strongly support the hypothesis that alterations in gastric emptying induced by AS and CS in mice are due to the release of CRF acting directly on central structures involved in the control of gastrointestinal motility.

Animals↗
PubMed2002

Gastric phytobezoar associated with impaired gastric motility in a patient with spinal cord injury.

Impaired gastrointestinal motility as a result of interruption of sympathetic outflow is a common occurrence in the spinal cord injury (SCI) population. In addition, frequent use of medications with anticholinergic properties in this population results in further impairment of peristalsis resulting in gastrointestinal stasis. Since SCI patients often lack sensation below the level of injury, they may present with vague symptoms, which complicates the diagnosis of intestinal obstruction. We report the first case of gastric phytobezoar in a patient with T4 ASIA A paraplegia who presented with vague upper abdominal discomfort, anorexia, weight loss, and vomiting. Because mortality rates can be as high as 30% if phytobezoars remain untreated, gastrointestinal phytobezoars should be considered in the differential diagnosis of abdominal discomfort in SCI patients. Etiologic factors for phytobezoars are discussed for the general population and in particular, for patients with SCI.

Bezoars↗