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PubMed1995

Effects of somatostatin on human satiety.

Somatostatin (ST) inhibits gastrointestinal motility and exocrine and endocrine secretions. In animals, ST has been demonstrated to decrease food intake. We investigated, in a randomized double-blind investigation in 10 healthy humans, the effects of an intravenous ST infusion compared to saline on subjective hunger feelings. After 1 h, a low dose of fat was given intraduodenally to induce the release of endogenous upper-intestinal satiety factors. Ninety minutes later sandwiches were served and eaten until satiation. In the first hour, when no intraduodenal fat was given, there was a significant decrease in feelings of hunger with ST (p < 0.05). During the intraduodenal fat infusion this pattern reversed with a trend towards less satiety with ST. Food intake during intraduodenal fat infusion tended to be higher during ST (305 +/- 42 g) than during saline (205 +/- 36 g) although not significantly. In the 5 h after the experiment hunger feelings were significantly less after ST. In conclusion, we found evidence for a satiety effect of ST in humans which reversed towards less satiety when intraduodenal intralipid, which presumably produced endogenous satiety factors, was given. Postmeal satiety is higher after ST.

Adult↗
PubMed1996

Symptom improvement from prokinetic therapy corresponds to improved quality of life in patients with severe dyspepsia.

Prokinetic therapy has been shown to improve patients' symptoms associated with gastrointestinal motility disorders and quality of life. This study investigated the correlation between clinical improvement and quality of life after 12 months of treatment with cisapride or domperidone in patients with severe dyspepsia. Psychological and quality-of-life measures were assessed at baseline and after 12 months of therapy using three patient-administered, standardized questionnaires: the Minnesota Multiphasic Personality Inventory, the Millon Behavioral Health Inventory, and the Sickness Impact Profile. Changes in clinical symptoms were correlated with changes in these measures. Twenty-seven patients with symptoms of severe dyspepsia were treated with cisapride or domperidone (60-80 mg/day) for 12 months. Symptoms and quality-of-life measures were improved at the end of therapy. There were significant correlations between improvement in clinical symptoms and improvement in quality of life parameters. Patients with more marked symptom improvement had more significant improvements in quality of life measures. We conclude that prokinetic therapy improved symptoms and quality of life. Standardized questionnaires can be used to quantify response to prokinetic therapy and to individualize treatment regimens for patients with dyspepsia who have specific psychologic or behavioral characteristics.

Adult↗
PubMed1989

Pharmacological characterization of morphine-6 beta-glucuronide, a very potent morphine metabolite.

Morphine-6 beta-glucuronide is a major metabolite of morphine with potent analgesic actions. To define more fully the importance of this compound in morphine action, we have compared the analgesic actions of morphine and its 6 beta-glucuronide metabolite after both peripheral and central administration. Given s.c., morphine-6 beta-glucuronide elicited analgesia with an effect approximately twice that of morphine due, in part, to its long duration of action and also inhibited gastrointestinal motility. Both actions were easily reversed by naloxone (s.c.). However, when injected either i.c.v. or intrathecally, morphine-6 beta-glucuronide was approximately 90- and 650-fold more potent an analgesic than morphine, respectively. Whereas morphine in these studies was equipotent at both levels of the neuraxis as an analgesic, the 6 beta-glucuronide was approximately 5-fold more effective at the level of the spinal cord than supraspinally. The mu 1-selective antagonist naloxonazine blocked the analgesic effect of systemic and i.c.v. morphine-6 beta-glucuronide much as it blocked morphine, implying a role for mu1 receptors in these actions. Like morphine, morphine-6 beta-glucuronide analgesia after intrathecal injection was not sensitive to naloxonazine, suggesting a mu2 mechanism within the spinal cord. Together, these results imply that morphine-6 beta-glucuronide elicited its analgesic actions through the same receptor mechanisms as morphine. Mice highly tolerant to morphine after implantation of morphine pellets showed cross-tolerance to morphine-6 beta-glucuronide (s.c.). The high potency of morphine-6 beta-glucuronide strongly suggests that this metabolite plays an important role in morphine's actions.

Analgesia↗
PubMed1989

Gastrointestinal motor patterns: motilin as a coordinating factor.

Our aim was to further define the role of neural and hormonal control of upper gastrointestinal motility patterns. In five dogs, the stomach and duodenum were separated enterically by transecting and oversewing the proximal duodenum and by anastomosing a Roux-en-Y jejunal limb to the pylorus. Five intact dogs served as controls. After recovery, motility was recorded on four or more occasions during fasting and after feeding. Plasma was sampled for motilin radioimmunoassay. In three Roux-en-Y dogs, motilin (0.1 microgram/kg iv) was administered. We found in the Roux-en-Y group that the characteristic MMC occurred in the stomach, duodenum, and jejunal limb, but the jejunal MMC had a much shorter period (P less than 0.005). Gastric and duodenal MMCs were coordinated temporally and were associated with peaks in plasma motilin concentration. Jejunal MMCs had no apparent association with plasma motilin. Feeding disrupted the gastric and duodenal MMC and decreased plasma motilin, but inhibited the jejunal MMC in only 6 of 12 experiments. Exogenous motilin induced a "premature" MMC in the stomach, duodenum, and jejunum. This study suggests that (1) enteric neural continuity and/or luminal continuity are not necessary for coordination of gastric and duodenal motor patterns, and (2) post-prandial inhibition of the duodenal MMC may not depend on the presence of ingested nutrient in the duodenum. Hormonal factors, possibly motilin, may play a role in initiation and coordination of gastric and duodenal motor patterns.

Anastomosis, Roux-en-Y↗
PubMed2004

Visceral hyperalgesia and intestinal dysmotility in a mouse model of postinfective gut dysfunction.

BACKGROUND & AIMS: We established the concept that transient enteric infection may lead to persistent gut dysfunction, evident in vitro, in nematode-infected mice. The present study determined whether gut dysfunction in this model involves motor and sensory changes reminiscent of changes found in patients with postinfective irritable bowel syndrome (PI-IBS) and investigated underlying mechanisms. METHODS: Mice infected up to 70 days previously with Trichinella spiralis (Tsp) underwent videofluoroscopy with image analysis to assess upper gastrointestinal motility. Pseudoaffective responses to colorectal distention (CRD) were assessed using a barostat and validated by single fiber recordings from spinal nerves during CRD. Tissues were examined at different time points for histology, immunohistochemistry, and cytokine analysis. Some mice received dexamethasone intraperitoneally on days 23-25 PI or Tsp antigen orally on days 29, 43, and 57 PI. RESULTS: From day 28 PI, no discernible inflammation was present in the gut. Frequency and propagation velocity of intestinal contractions decreased, and retroperistalsis increased at days 28 to 42 PI. CRD induced an allodynic and hyperalgesic response in PI mice, which was accompanied by increased single unit discharge. Gavage of Tsp antigen induced T-cell responses and sustained gut dysfunction for 70 days PI. Administration of dexamethasone postinfection normalized dysmotility and visceral hyperalgesia. CONCLUSIONS: Long-lasting gut dysmotility and hyperalgesia develop in mice after transient intestinal inflammation. These changes are maintained by luminal exposure to antigen and reversed by corticosteroid treatment. The findings prompt consideration of this as a model of PI-IBS.

Animals↗
PubMed2001

Blockade of GRP receptors inhibits gastric emptying and gallbladder contraction but accelerates small intestinal transit.

BACKGROUND & AIMS: This study was designed to characterize [D-F(5)Phe(6)D-Ala(11)]Bn(6-13)OMe (BIM26226) as a gastrin-releasing peptide (GRP)-preferring bombesin receptor antagonist and to determine whether GRP physiologically regulates gastrointestinal motility. Intravenous BIM26226 (5-500 microg. kg(-1). h(-1)) inhibits GRP-induced gallbladder contraction and plasma cholecystokinin (CCK) release in a dose-dependent fashion. METHODS: Gastric emptying and small bowel transit of a solid meal were quantified using scintigraphy. Meal-stimulated gallbladder contraction was measured by sonography in a 2-period crossover design. RESULTS: Intravenous BIM26226 potently inhibited gastric lag time (114 +/- 7 vs. 41 +/- 6 minutes [control]) and gastric emptying rate (0.11 +/- 0.02%/min vs. 0.26 +/- 0.04%/min [control]), whereas concomitant infusion of BIM26226 accelerated small bowel transit time (153 +/- 41 vs. 262 +/- 20 minutes [control]). A continuous liquid meal perfusion into the duodenum induced complete gallbladder contraction (t(50%), 35 +/- 4 minutes), which BIM26226 inhibited significantly (t(50%), 64 +/- 8 minutes). BIM26226 did not alter plasma CCK response, indicating that circulating CCK did not mediate these effects. CONCLUSIONS: These data show that BIM26226 is a potent antagonist of exogenous and endogenous GRP and suggest that GRP is a major physiologic regulator of gastric emptying, small bowel transit, and gallbladder contraction.

Adult↗
PubMed1989

Effects of a 5-hydroxytryptamine3 receptor antagonist (ICS 205-930) on colonic motor activity in healthy men.

1. ICS 205-930 (Sandoz) is a selective antagonist at 5-hydroxytryptamine3 receptors and exerts marked effects on gastrointestinal motility in animals. 2. This study investigated, under random double-blind conditions, the effects of 10 and 20 mg ICS 205-930 infused intravenously in comparison with placebo on colonic motor activity. 3. Twelve healthy men participated each in three studies in which they received, in random double-blind fashion, each of the treatments. Colonic pressures were recorded pneumohydraulically with four catheter orifices 20-40 cm from the anal verge. Treatments were administered after a basal 30 min. One hour later, subjects ingested a 4200 kJ meal and 90 min thereafter, 1 mg neostigmine was administered intramuscularly and recording continued for another 90 min. 4. After both doses of ICS 205-930, the number of contractions as averaged over the entire recording time was slightly but significantly higher than after placebo. 5. After 10 mg but not after 20 mg ICS 205-930, amplitude of contractions and area under the curve as averaged over the entire recording time were significantly higher than after placebo. 6. ICS 205-930 induced few and mild side effects, but significantly more self-rated drowsiness and tiredness than placebo.

Adult↗
PubMed1997

Effect of nitric oxide synthase inhibition on plasma motilin release in fasted dogs.

Inhibition of nitric oxide (NO) synthase on plasma motilin concentrations is not known. The aim of this study was to examine the effect of NO synthesis inhibitor on gastrointestinal motility and motilin release in conscious dogs. Dogs fitted with force transducers were given N omega-nitro-L-arginine (L-NNA) after the termination of phase III contractions. Blood samples were taken for measurement of motilin concentrations. L-NNA induced phase III-like contractions in the stomach in the duodenum in association with a significant increase in motilin level. Atropine or hexamethonium significantly inhibited L-NNA-induced phase III-like contractions and the increase in motilin level. Atropine or hexamethonium significantly inhibited L-NNA-induced phase III-like contractions and the increase in motilin level. Ondansetron markedly inhibited gastric, but not duodenal, phase III-like contractions without affecting the increase in motilin level caused by L-NNA. Vagotomy affected neither the occurence of phase III-like contractions nor the increase in motilin level produced by L-NNA. We conclude that inhibition of NO synthesis stimulates motilin release via cholinergic pathways independent of the vagus, and induces phase III-like contractions in the stomach and duodenum. Phase III-like contractions induced by L-NNA are mediated through the activation of 5-HT, receptors.

Animals↗
PubMed1984

Effects of oral cyclotropium bromide, hyoscine N-butylbromide and placebo on gastric emptying and antral motor activity in healthy man.

Cyclotropium bromide, a new antimuscarinic agent, inhibits gastrointestinal motility in animals at lower doses than those required to inhibit gastric acid secretion and salivation. In man, cyclotropium bromide suppresses fasting and meal stimulated colonic motility. This study investigated the effects of single oral doses of 60 mg cyclotropium bromide, 60 mg hyoscine N-butylbromide and placebo on gastric emptying and on antral motor activity. Twenty four healthy men (mean age 25 years) participated in three experiments one week apart. The drugs were administered, in random double blind fashion, 30 minutes before the ingestion of a semisolid test meal labelled with 74 MBq (2 mCi) 99mTc sulphur colloid. A gamma camera coupled to a computer monitored gastric emptying together with amplitude, frequency, and propagation velocity of antral contractions. Cyclotropium bromide and, to a lesser degree, hyoscine N-butylbromide delayed gastric emptying and reduced contraction amplitude, but did not affect frequency and propagation velocity of antral contractions. Cyclotropium bromide was significantly more active than hyoscine N-butylbromide; the effects of hyoscine N-butylbromide differed significantly from placebo. Antral contractile activity was present all the time. After cyclotropium bromide, there was a significant correlation between antral contraction amplitude and gastric emptying. No adverse side effects occurred with any one treatment. In conclusion, cyclotropium bromide markedly inhibits gastric emptying and reduces antral contraction amplitude.

Adult↗
PubMed1987

Frequency analysis of gut EMG.

The EMG of the gut smooth muscle plays an important role in the regulation of gastrointestinal motility in health and disease. The EMG in general consists of an omnipresent oscillatory electrical control activity (ECA) and spikes or other potentials that result in contractions of the smooth muscle. This paper addresses the question of how the ECA signals can best be processed and how inappropriate transformations of such signals may produce misleading results. The various factors affecting the composition of the gut EMG, in time and space along the gut, are discussed briefly. The need for the analysis of the ECA for its oscillatory nature is mentioned together with details regarding the widely used visual, period, and Fourier analysis techniques. Fourier analysis techniques have been applied with increasing frequency to gut EMG; the various features of Fourier analysis and considerations for their implementation on the computer are discussed. The visual, period, and Fourier analysis approaches as well as their uses and limitations in application to a variety of ECAs of the stomach and of the colon in dogs and humans are illustrated. This study indicates that period analysis techniques are well suited for the study of the visibly oscillatory upper gut EMG, while smoothed spectral analysis is more appropriate for the study of colonic EMG.

Animals↗
PubMed1985

The relation between food intake and abomasal emptying and small intestinal transit time in sheep.

The relation between the level of food intake and gastrointestinal motility and digesta flow in the abomasum and small intestine was studied in sheep fitted with nichrome-wire electrodes in the gut wall, an abomasal and a duodenal catheter and a terminal ileal cannula. Abomasal volume and outflow were calculated from CrEDTA dilution in six sheep and small intestinal transit time by the passage of Phenol Red in ten sheep. The frequency of the migrating myoelectric complex of the small intestine was not altered by the level of food intake but the duration of the periods of irregular spiking activity, the amplitude of abomasal activity and the frequency of duodenal rushes were decreased as the level of food intake was decreased. There was a linear relation between the level of food intake (FI) and abomasal outflow (mean with SEM: 327 (69) ml/h for each kg FI/d; P less than 0.01), and abomasal volume (mean with SEM: 344 (50) ml/kg FI per d; P less than 0.001), without any significant change in the half-time of marker dilution in the abomasum. Small intestinal transit time decreased with an increase in food intake (mean with SEM: -54.9 (5.6) min/kg FI per d; P less than 0.001). It is concluded that abomasal volume and the rate of digesta flow from the abomasum and along the small intestine are linearly related to the level of food intake.

Abomasum↗
PubMed1990

Oral prostaglandin E analogues induce intestinal migrating motor complexes after a meal in dogs. Evidence for a central mechanism.

The effects of oral, intravenous, and intracerebroventricular administration of synthetic derivatives of prostaglandins E1 (misoprostol) and E2 (enprostil) on postprandial gastrointestinal motility were investigated in dogs chronically fitted with strain gauge transducers on the antrum and the proximal and middle jejunum. Synthetic prostaglandin E analogues administered orally at a dose of 20-50 micrograms/kg 15 min before the meal did not modify the postprandial pattern of gastric contractions but suppressed the spontaneous postprandial irregular activity on the jejunum and induced a cyclic pattern of migrating motor complexes for 4-6 h after the meal. These postprandial migrating motor complexes induced by prostaglandin E were propagated between the two recording sites and had a period similar to that observed in the fasted state. However, the duration of phase 2 was significantly increased and the amplitude of the phase 3 decreased. This jejunal cyclic motor pattern was reproduced by administration of synthetic prostaglandin E derivatives either intravenously (4-10 micrograms/kg) 15 min before the meal or intracerebroventricularly (50 ng/kg) 1 h after the meal. The intestinal migrating motor complex activity observed after oral administration of synthetic prostaglandin E derivatives was abolished by the previous intracerebroventricular (40 micrograms/kg) but not intravenous (200 micrograms/kg) administration of SC-19220, a receptor antagonist of prostaglandin E. These results suggest that oral administration of synthetic prostaglandin E1 (misoprostol) or prostaglandin E2 (enprostil) analogues before a meal induces postprandial migrating motor complexes on the jejunum in dogs through a mechanism involving central prostaglandin receptors.

Administration, Oral↗
PubMed1995

Effect of antrectomy and truncal vagotomy on erythromycin induced pancreatic polypeptide secretion.

Erythromycin, a motilin agonist, enhances gastrointestinal motility but also stimulates endogenous pancreatic polypeptide (PP) secretion. We investigated whether the effect of erythromycin on PP release is dependent on (1) prokinetic activity of erythromycin generated from the antrum and (2) the long vagus nerve since erythromycin acts via cholinergic neurons. Erythromycin induced PP secretion was determined in 14 patients with antrectomy (6 patients with Billroth I type anastomosis, 8 patients with Billroth II type anastomosis), in 6 patients with truncal vagotomy and pyloroplasty but without gastric resection and in 8 healthy controls. Plasma PP levels in response to erythromycin (3 mg/kg i.v.) were determined at regular intervals for 180 min. Erythromycin induced a significant increase in plasma PP in the control subjects from 22 +/- 4 pmol/l (basal) to 49 +/- 4 pmol/l at 10 min. In the patients with truncal vagotomy plasma PP secretion after erythromycin was significantly (P < 0.05) increased (peak increment vs. basal: 98 +/- 10 pmol/l vs. 27 +/- 2 pmol/l) and prolonged compared to controls. In the patients with antrectomy no significant increases in plasma PP over basal were observed after erythromycin infusion. It is concluded that erythromycin stimulates PP secretion in healthy controls. The PP response to erythromycin is exaggerated after truncal vagotomy but absent after antrectomy indicating that the antrum is essential for erythromycin induced PP secretion.

Adult↗
PubMed1990

Substance P and CGRP mediate motor response of rabbit colon to capsaicin.

Primary afferent nerve terminals located in the mammalian gut wall may play a role in region-specific modulation of gastrointestinal motility. In the present study, we sought to characterize the effect of neuropeptides released from these afferents by capsaicin (CAP) on contractile activity of smooth muscle from the distal rabbit colon. CAP caused a release of acetylcholine and immunoreactivity for substance P (SP) and calcitonin gene-related peptide (CGRP) from the muscle coat. CAP caused a dose-dependent transient stimulation of longitudinal muscle contractions, followed by prolonged inhibition of spontaneous but not stimulated contractile activity. The initial stimulation was abolished by the SP antagonist spantide and by atropine. The inhibitory effect was reduced by repeated exposure of muscle to CGRP. The effect of CGRP on spontaneous contractions differed between longitudinal and circular muscle. In longitudinal muscle, a stimulation was preceded by a transient inhibition, whereas in circular muscle, only inhibition was seen. Both effects were resistant to tetrodotoxin. Repeated exposure of circular but not longitudinal muscle to CGRP resulted in a disappearance of the peptide's inhibitory effect. Exogenously applied CGRP was only a weak antagonist of contractions stimulated by SP and bethanechol. These findings suggest that in the rabbit colon at least the following two neuropeptides are released from CAP-sensitive nerve fibers: a neurokinin peptide from nerve terminals located within the myenteric plexus and CGRP from terminals probably located within the circular muscle layer.

Acetylcholine↗
PubMed2005

alpha- and beta-adrenergic receptor mechanisms in spontaneous contractile activity of rat ileal longitudinal smooth muscle.

Gastrointestinal motility is influenced by adrenergic modulation. Our aim was to identify specific subtypes of adrenergic receptors involved in inhibitory mechanisms that modulate gut smooth muscle contractile activity. Muscle strips of rat ileal longitudinal muscle were evaluated for spontaneous contractile activity and for equimolar dose-responses (10(-7) to 3 x 10(-5) M) to the adrenergic agents norepinephrine (nonselective agonist), phenylephrine (alpha(1)-agonist), clonidine (alpha(2)-agonist), prenalterol (beta(1)-agonist), ritodrine (beta(2)-agonist), and ZD7114 (beta(3)-agonist) in the presence and absence of tetrodotoxin (nonselective nerve blocker). Norepinephrine (3 x 10(-5) M) inhibited 65 +/- 6% (mean +/- SEM) of spontaneous contractile activity. The same molar dose of ritodrine, phenylephrine, or ZD7114 resulted in less inhibition (46 +/- 7%, 31 +/- 5%, and 39 +/- 3%, respectively; P < 0.05). The calculated molar concentration of ZD7114 needed to induce 50% inhibition was similar to that of norepinephrine, whereas higher concentrations of phenylephrine or ritodrine were required. Clonidine and prenalterol had no effect on contractile activity. Blockade of intramural neural transmission by tetrodotoxin affected the responses to ritodrine and phenylephrine (but not to norepinephrine or ZD7114), suggesting that these agents exert part of their effects via neurally mediated enteric pathways. Our results suggest that adrenergic modulation of contractile activity in the rat ileum is mediated primarily by muscular beta(3)-, beta(2)-, and alpha(1)-receptor mechanisms; the latter two also involve neural pathways.

Adrenergic alpha-Agonists↗
PubMed1992

Pharmacokinetic interactions of cefprozil with food, propantheline, metoclopramide, and probenecid in healthy volunteers.

Cefprozil, a new oral cephalosporin antibiotic, is composed of cis and trans isomers in an approximate 90:10 ratio. The objectives of this study were: (1) to assess the effects of alterations in gastrointestinal motility by metoclopramide and propantheline on the pharmacokinetics of cis and trans isomers of cefprozil, and to compare them with the effects of food on the pharmacokinetics of cefprozil; (2) to assess the effects of inhibition of renal tubular secretion by probenecid on the pharmacokinetics of cefprozil isomers. In this four-way crossover study, 15 healthy male volunteers received a 1000-mg dose of cefprozil after fasting, pretreatment with metoclopramide or propantheline, after breakfast, or after probenecid in an incomplete, balanced block design. There was a 1-week washout period between each treatment. Blood and urine samples collected over a 24-hour period were assayed for the cis and trans isomers. The concentrations of the trans isomers were generally 1/10 of the cis isomer. The means and variances of the pharmacokinetic parameters of the cis and trans isomers of cefprozil were similar in fasting subjects and were affected in a parallel manner by food, metoclopramide, propantheline, and probenecid. The pharmacokinetics of the cis isomer under the fasting condition were as follows: maximum peak plasma concentration (Cmax), 14.0 +/- 2.7 micrograms/mL; median time to reach Cmax (tmax), 1.5 (range, 1.0-3.5) hours; half-life (t1/2), 1.24 +/- 0.27 hours; area under the concentration (AUC0-infinity), 47.3 +/- 7.7 micrograms.hour/mL; mean residence time after oral administration (MRTpo), 2.9 +/- 0.4 hours; CLR, 219 +/- 60 mL/minute; and Xu% (percent cumulative urinary excretion in 0-24 hours), 68.1 +/- 12.5.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

Differential effects of progesterone and its analogues on the contractility of the murine jejunum in vitro.

Epidemiological studies have demonstrated a higher prevalence of gastrointestinal motility disturbances in women compared with men. This may partly be due to the effects of sex hormones on smooth muscle cells. To further characterize the mechanisms by which sex hormones affect intestinal smooth muscle, we studied the effects of several structurally related progestins on intestinal contractility. Segments of the murine intestine oriented along the longitudinal axis were connected to force displacement transducers. We recorded the isometric tension generated by the murine jejunum spontaneously and after cholinergic stimulation. The baseline tension, amplitude of spontaneous contractions, and increase in tension after cholinergic stimulation were measured in the presence and absence of various steroid hormones. Progesterone dose dependently decreased the contractile activity of the murine jejunum. This effect occurred within less than 1 min and could not be inhibited by a specific blocker of the progesterone receptor, suggesting a nongenomic pathway. Experiments with several progestins demonstrated a stereoselectivity of this steroid hormone effect. This was most pronounced for dihydroprogesterone: the 5 alpha form did not affect intestinal contractility, while the stereoisomer 5 beta-dihydroprogesterone significantly inhibited smooth muscle tension. We conclude that progesterone significantly inhibits the contractility of the murine jejunum in vitro. The differential effects of various structural analogues argue against a nonspecific effect of the steroid hormones on the lipid bilayer with secondary functional alterations of membrane proteins. Rather, they suggest a specific interaction between the steroid hormone and a still unidentified protein that differs in its function and pharmacological profile from the known progesterone receptor.

20-alpha-Dihydroprogesterone↗
PubMed1999

Dopamine reduces gastric tone in a dose-related manner.

BACKGROUND: Dopamine may have effects on gastrointestinal motility. The aim of this study was, therefore, to determine whether dopamine reduces gastric tone and whether the effects of dopamine can be blocked by a dopamine antagonist. METHODS: Eight healthy male volunteers were studied on two occasions in a randomized order. A continuous infusion of incremental doses of dopamine (2.5, 5.0, 7.5 microg kg(-1) min(-1)) was given on both occasions. Ten milligrams of the dopamine-antagonist metoclopramid was given before the dopamine infusion on one occasion and during the dopamine infusion (7.5 microg kg(-1) min(-1)) on the other occasion. The gastric tone was measured by an electronic barostat, an instrument with an electronic control system that maintains a constant preset pressure within an air-filled, flaccid intragastric bag by means of momentary changes in the intragastric volume of air. Volume and pressure in the gastric bag were continuously recorded by the electronic barostat and sampled in a computer. RESULTS: Dopamine induced a dose-related increase in the intragastric bag volume. Metoclopramid given as a 10 mg i.v. bolus dose during the infusion of dopamine significantly decreased the intragastric bag volume, but 10 mg of metoclopramid i.v. before the dopamine infusion did not influence the bag volume per se. CONCLUSION: Dopamine decreases gastric tone in a dose-related manner and 10 mg of the dopamine-antagonist metoclopramid is not enough to fully reverse these effects.

Adult↗