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Biomedical subjects

J Fioramonti

Publications and source records attributed to J Fioramonti.

At least 109 records · Page 6Linked to original sources
PubMed1994

Induction of postprandial intestinal motility and release of cholecystokinin by polyamines in rats.

Polyamines are known to play a major role in postprandial adaptation of the digestive tract. Experiments were designed to determine whether ingested polyamines induce change in intestinal motility associated with a cholecystokinin (CCK) release and whether endogenous polyamines are involved in the intestinal and colonic motor response to a meal. Intestinal and colonic motility was assessed in rats equipped with intestinal electrodes, and plasma CCK was determined using a bioassay. Orogastric administration of putrescine, spermidine, or spermine (20 mumol) disrupted intestinal migrating myoelectric complexes (MMCs) and increased the frequency of colonic spike bursts. After a 6-day treatment with the ornithine decarboxylase inhibitor alpha-difluoromethylornithine, the duration of postprandial disruption of MMCs, but not the stimulation of colonic motility, induced by a 3-g meal was significantly reduced. The duration of MMC disruption and the increase in colonic spike burst frequency after spermidine administration (20 mumol) were significantly reduced by CCK-A and CCK-B antagonists. Eight minutes after saline administration plasma CCK concentration was 0.9 +/- 0.4 pM; it rose to 4.7 +/- 2.8 pM, 8 min after spermidine (20 mumol). These results indicate that exogenous polyamines disrupt intestinal MMCs and stimulate colonic motility through a release of CCK acting at CCK-A and CCK-B receptors and suggest that endogenous polyamines are involved in the postprandial control of intestinal motility.

Animals↗
PubMed1993

Stimulatory (EP1 and EP3) and inhibitory (EP2) prostaglandin E2 receptors in isolated ileal smooth muscle cells.

Isolated smooth muscle cells from the circular layer of pig and guinea-pig ileum were used to study the effect of prostaglandin E2 (PGE2) and three PGE2 receptor (EP) agonists; iloprost (EP1), butaprost (EP2) and enprostil (EP3). In pig cells, PGE2 and enprostil induced cell contraction (22.1 and 21.5% shortening of cell length, obtained at 10 nM for PGE2 and 1 nM for enprostil, respectively). Iloprost and butaprost had no contractile effect. However, the cholecystokinin octapeptide (CCK-8; 10 nM)-induced contraction was inhibited when cells were preincubated with iloprost or butaprost. In guinea-pig cells, PGE2, butaprost and iloprost induced cell contraction, whereas enprostil had no effect (23.1% for 10 nM PGE2, 22.8% for 1 nM butaprost and 22.6% for 10 nM iloprost). Preincubation with SC19220 (EP1 antagonist) inhibited the PGE2-, butaprost- and iloprost-induced contractions. When the contractile effect of PGE2, butaprost and iloprost was inhibited by addition of SC19220, these agents inhibited the cell contraction induced by CCK-8 (1 nM). Smooth muscle cells from guinea-pig and pig ileum express two PGE2 receptor subtypes that induce opposite effect. EP1 and EP3 receptors mediate cell contraction in guinea-pig and pig, respectively, whereas EP2 receptors mediate cell relaxation in both species.

Alprostadil↗
PubMed1993

Central and peripheral serotonergic influences on viscerovisceral inhibitory reflex during duodenal distension in sheep.

The effects of duodenal distension on forestomach and abomasal motility were investigated in conscious sheep chronically fitted with intraparietal electrodes, a duodenal cannula, and an intracerebroventricular cannula. Duodenal distensions with a balloon inflated with 40 ml (DD40) of water reduced the frequency of forestomach and abomasal contractions by 45 and 32%, respectively, while distension with 80 ml (DD80) induced a total inhibition. Methysergide, a mixed 5HT1-5HT2 antagonist administered intravenously (200 micrograms/kg) or intracerebroventricularly (20 micrograms/kg) suppressed the DD40-induced inhibition and reduced that induced by DD80. Spiroxatrine, a selective 5HT1A antagonist, intravenously (100 micrograms/kg) or intracerebroventricularly (10 micrograms/kg), suppressed the DD40 and DD80-induced inhibition, which was also attenuated by the 5HT2 antagonist ritanserin given intravenously (200 micrograms/kg) or intracerebroventricularly (20 micrograms/kg). Granisetron, a 5HT3 antagonist, injected intravenously (150 micrograms/kg), abolished the effects of DD40 and DD80 while it had no antagonistic action on DD40 and DD80 when given intracerebroventricularly (15 micrograms/kg). It is concluded that in sheep, duodenal distension inhibits forestomach and abomasal motility through 5HT1A and 5HT2 receptors at the level of the central nervous system and 5HT3 receptors located peripherally.

Animals↗
PubMed1993

Central action of interleukin 1 beta on intestinal motility in rats: mediation by two mechanisms.

BACKGROUND: Interleukin 1 (IL-1) can influence gut functions by inhibiting gastric acid secretion. This study was performed to investigate the effects of IL-1 on intestinal motility and the mechanisms involved. METHODS: The effects of IL-1 beta were determined by electromyography in conscious rats with implanted electrodes and a permanent catheter in a lateral brain ventricle. RESULTS: Intracerebroventricular IL-1 beta (15 ng) administered to fed rats immediately stimulated cecocolonic spike bursts and caused a migrating myoelectric complex pattern after a delay in the small intestine. Tenfold higher doses of peripherally administered IL-1 beta did not promote similar reactions. The IL-1 antagonist reduced the small intestinal effect of IL-1 beta and blocked the cecocolonic stimulation. Indomethacin and SC 19220 reduced the small intestinal effects but did not antagonize the increase in cecocolonic contractions. In contrast, alpha-helical CRF9-41 blocked the increase of cecocolonic contractions but did not antagonize the IL-1 beta-induced effects on the small intestine. CONCLUSION: IL-1 beta's effects on intestinal motility can be mainly ascribed to a central action. The cecocolonic stimulation may be mediated by brain corticotropin-releasing factor, whereas the small intestinal effects involve a prostaglandin mediation.

Animals↗
PubMed1993

Recombinant interleukin-1 receptor antagonist protein prevents sensitization and intestinal anaphylaxis in guinea pigs.

Recombinant interleukin-1 receptor antagonist protein (rlRAP, 0.5 mg/kg) administered intraperitoneally in guinea pigs one hour before primary and booster parenteral sensitization (1 ml) by cow milk, led to a reduced immunoglobulin E (IgE) production, as displayed by a passive cutaneous anaphylaxis test. rlRAP administered intraperitoneally in sensitized guinea pigs at 0.5 mg/kg 10 min before challenge administration (beta-lactoglobulin, 100 mg per os), also prevents the colonic motor and secretory changes induced by intestinal anaphylaxis. These results suggest the involvement of interleukin-1 in food allergy and evidence a double protective role for rlRAP in food hypersensitivity.

Anaphylaxis↗
PubMed1993

In vivo motility of rat colon chronically pretreated with sennosides.

Ceco-colonic myoelectrical activity was investigated in rats pretreated for 23 weeks by sennosides (10 or 40 mg/kg/day), Na-picosulfate (2.5 or 10 mg/kg/day) or laxative vehicle (control). On the last week of treatment the animals were equipped with Nichrome electrodes on the cecum, the proximal and distal colon. In comparison with controls, sennoside or Na-picosulfate treatment did not induce any significant (p > 0.05) change in the duration of long spike bursts (LSB) which are associated with phasic contractions. On the last 2 days of treatment the frequency of LSB for 2 h before and 2 h after laxative administration, as well as for 30 min after a 3-gram meal was not significantly (p > 0.05) different in control and treated animals. Similarly, on the first 2 days, as well as on days 13 and 14, after the end of treatment, no significant (p > 0.05) difference in the LSB frequency appeared between control and treated animals, in the fasted state or after a 3-gram meal. It is concluded that long-term treatment with sennosides or Na-picosulfate does not induce chronic changes in colonic motility in rats.

Animals↗
PubMed1993

Involvement of capsaicin-sensitive afferent nerves in the intestinal motor alterations induced by intestinal anaphylaxis in rats.

Alteration of intestinal myoelectrical activity is a characteristic feature of food protein-induced intestinal anaphylaxis in the conscious rat. The motility changes induced by antigen challenge were appraised in egg-albumin-sensitized rats, chronically implanted with NiCr electrodes in the duodenojejunal wall. Intraduodenal infusion of egg albumin given to fasted sensitized rats triggered a disruption of the cyclic pattern of small intestinal motility lasting 79.1 +/- 23.3 min. The duration of the challenge effect on intestinal myoelectrical activity was significantly reduced by systemic capsaicin pretreatment (125 mg/kg) but to a lesser extent by perivagal capsaicin. Substance P (SP) antagonists (SP 4-11 and CP 96.345) and atropine were also able to shorten the duration of the antigen-challenge-induced alteration of intestinal motility. It is concluded that SP and capsaicin-sensitive afferent nerve endings play an important role in the intestinal anaphylaxis-induced disturbances of intestinal motility.

Afferent Pathways↗
PubMed1993

[Role of serotonin and histamine in the effects of degranulation of mast cells on the colonic motility and the transit. Experimental study in rats].

The aim of this work was to describe the alterations of colonic motility and transit induced by an experimental, histologically verified, degranulation of mast cells, provoked by the compound BrX-537A, and to determine the role of serotonin and histamine by specific antagonists, in the rat. Colonic myoelectrical activity was inhibited by BrX-537A (2 mg/kg IP) in a biphasic manner. The initial profound inhibition, lasting 30 min, during which the frequency of spike bursts decreased from 9.2 +/- 1.1 to 1.4 +/- 0.5/10 min, was followed by a sustained (5 h) period of moderate inhibition (5.2 +/- 0.5 spike bursts/10 min). In the same way, BrX-537A increased the mean retention time of a marker injected in the proximal colon (10.8 +/- 1.4 h vs 7.4 +/- 0.4 h). Neither serotoninergic nor histaminergic antagonists, at a dose of 1 mg/kg IP, modified the primary drastic inhibition of colonic motility during the first 20 minutes. After, a selective time-related blockade of this inhibition was observed. Granisetron blocked the inhibition from the 30th minute on, methysergide from the 120th minute on, and chlorpheniramine, between the 20th and 60th minutes. In conclusion, the inhibitory effect of mast cell degranulation depends on serotonin and histamine release, in a time-related manner, and implicates the H1, 5-HT3 and 5-HT1 or 2 receptors.

Animals↗
PubMed1993

The mycotoxin, deoxynivalenol, delays gastric emptying through serotonin-3 receptors in rodents.

The effects of the trichotecene mycotoxin, deoxynivalenol, on gastric emptying and intestinal propulsion in mice and rats and gastrointestinal myoelectrical activity in rats were investigated. Gastric emptying and intestinal transit were evaluated after gavage with a milk meal containing a marker (51CrO4Na2) and radio-activity was counted in the stomach and 10 segments of the small intestine. The myoelectrical activity of the antrum, duodenum and jejunum was assessed by implanting electrodes for long-term electromyographic recordings. Deoxynivalenol given orally (50-1000 micrograms/kg) but not i.c.v. (5 micrograms/kg) 10 min before the test meal inhibited gastric emptying in a dose-related manner. Intestinal propulsion was reduced for the highest dose (1000 micrograms/kg) only. The inhibition of gastric emptying induced by deoxynivalenol was antagonized by ondansetron and granisetron given s.c. (50 micrograms/kg) but not by ondansetron i.c.v. (10 micrograms/kg). Metoclopramide, domperidone (1 mg/kg s.c.), methysergide, ritanserin and cisapride (2 mg/kg s.c.) did not modify the deoxynivalenol-induced inhibition of gastric emptying. In rats, gavage with a 2.5-ml milk meal increased the frequency of antral spike bursts from 1.9 +/- 0.9/min in the fasted state to 4.7 +/- 0.4/min and disrupted intestinal migrating motor complexes for 84.9 +/- 10.8 min. Oral administration of deoxynivalenol (50-100 micrograms/kg) 10 min before the meal did not modify the frequency of antral spike bursts but induced migrating motor complexes on the small intestine after the meal. This effect was reversed by ondansetron (10 micrograms/kg s.c.). It was concluded that, in rodents, deoxynivalenol inhibits gastric emptying by inducing intestinal migrating motor complexes through a peripheral action at the serotonin-3 receptors.

Animals↗
PubMed1993

Comparative action of Phe-Leu-Phe-Gln-Pro-Gln-Arg-Phe-NH2 analogs on intestinal motility and nociception in rats.

Central (i.c.v.) effects of D-Tyr-D-Leu-[N-Me]-Phe-Gln-Pro-Gln-Arg-Phe-NH2 [(1DME)Y8Fa] and D-Tyr-D-Leu-D-Phe-Gln-Pro-Gln-Arg-Phe-NH2 [(3D)Y8Fa], synthetic analogs of Phe-Leu-Phe-Gln-Pro-Gln-Arg-Phe-NH2 on intestinal myoelectric activity and nociception were studied and compared to that of D-Ala2-Met5-enkephalinamide in rats. The duration of disruption of intestinal migrating myoelectric complexes, induced by p.o. administration of a test meal was significantly shortened (P < .01) by (1DME)Y8Fa and (3D)Y8Fa (8, 40 and 80 micrograms/kg) and D-Ala2-Met5-enkephalinamide (40 and 80 micrograms/kg). The coadministration of any two of these drugs, at doses of nonmeasurable effect when given alone (2 micrograms/kg), has also reduced the duration (P < .01) of the postprandial intestinal motor profile. Both separate and combined effects of drugs were antagonized by naloxone (1 mg/kg s.c.). In contrast, in the tail-flick test, analgesia induced by D-Ala2-Met5-enkephalinamide (40 micrograms/kg i.c.v.) was blocked by (1DME)Y8Fa, (3D)Y8Fa (8 micrograms/kg) and naloxone (1 mg/kg s.c.). The coadministration of (1DME)Y8Fa and (3D)Y8Fa at doses of no proper effect when given alone (8 micrograms/kg) has significantly (P < .01) reduced the latency time. This effect was not blocked by naloxone (1 mg/kg s.c.). It is concluded that the Phe-Leu-Phe-Gln-Pro-Gln-Arg-Phe-NH2 analogs, (1DME)Y8Fa and (3D)Y8Fa, when given i.c.v. exert effects similar to opiate agonists and antagonists on intestinal myoelectrical activity and on nociception, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1992

Differences between jejunal myoelectric activity after a meal and during phase 2 of migrating motor complexes in healthy humans.

Using an intraluminal probe with six pairs of annular electrodes, the myoelectric activity of the proximal jejunum was recorded during 48-hr sessions in 16 healthy volunteers receiving evening and noon meals (1000 kcal) and breakfast (400 kcal). In 10 subjects receiving no drug, the characteristics of the migrating motor complexes (period, duration of each phase, velocity of propagation of phase 3, duration of the postprandial disruption) varied markedly between subjects but were relatively constant from the first to the second day of recording. Single spike bursts propagated at a rate of 2-5 cm/sec, clusters of 3-10 spike bursts propagated at a rate of 0.5-1 cm/sec, and similar clusters recurring repetitively each 1.5-2 min were observed after the meals and very rarely in the fasted state during phase 2 of nocturnal migrating motor complexes. In six subjects, oral administration of codeine (50 mg) 1 hr before a meal induced migrating motor complexes in the postprandial state, with characteristics similar to that observed in the fasted state except a longer duration of phase 2. Single spike bursts and isolated and repetitive clusters of spike bursts were observed during phase 2 of the codeine-induced migrating motor complexes and after meals preceded by placebo, but very rarely during the phase 2 of nocturnal (fasted state) migrating motor complexes. It is concluded that the patterns of jejunal contractions consisting of propagated single spike bursts and isolated or repetitive spike bursts characterize the postprandial state in healthy humans and are dependent upon digesta flow.

Adult↗
PubMed1992

Relationship between mast cell degranulation and jejunal myoelectric alterations in intestinal anaphylaxis in rats.

The effects of two degranulators of mast cells and intestinal anaphylaxis on jejunal myoelectric activity were compared in rats fasted for 15 hours. Attempts to antagonize the motility changes were performed using antagonists of histamine and serotonin and a cyclooxygenase and lipoxygenase inhibitor. Hooded Lister rats were chronically fitted with electrodes implanted in the jejunal wall. A group of rats was sensitized to egg albumin and challenged 14 days later by intraduodenal infusion of antigen. Sensitized animals had serum titers greater than or equal to 1:64. The other group was administered with mast cells degranulators. Both 48/80 (1 mg/kg), a degranulator of connective mast cells, and bromolasalocid (2 mg/kg), acting on connective and mucosal mast cells, induced a phase of total spiking inhibition followed by a progressive irregular spiking activity until the recovery of migrating myoelectric complex pattern (about 3 hours after injection). In contrast, antigen challenge disrupted the migrating myoelectric complex pattern, which was replaced by a peculiar pattern characterized by propagated spike burst, lasting 98 +/- 11.3 minutes. Chlorpheniramine (1 mg/kg) antagonized only the inhibitory phase induced by degranulators and was ineffective on the intestinal anaphylaxis-induced motor changes. Methysergide (1 mg/kg) and indomethacin (5 mg/kg) significantly reduced the degranulator effects as well as the anaphylaxis-induced alterations of intestinal motility. It is concluded that anaphylaxis-induced motor disturbances are relevant to mucosal mast cell degranulation involving 5-hydroxytryptamine and arachidonic acid derivative products, whereas histamine release appears to be a minor component.

Anaphylaxis↗
PubMed1992

Aluminium hydroxide uptake in the stomach and in the intestine of the rat: a histochemical study.

Using the histochemical stains aluminon, solochrome azurine and solochrome cyanine, intracellular binding of aluminium was examined in the mucosa of the stomach, duodenum, jejunum and ileum of adult rats. A first group of rats (n = 42) was sacrificed 1, 3, 6, 12, 24, 48 and 96 h after a single (300 mg x kg-1) oral administration of aluminium hydroxide. A second group of animals (n = 30) received daily the same dose of Al(OH)3 and was euthanatized after 3, 4, 5, 6 and 7 days of treatment. Aluminium deposits occurred only in the antral glands of the stomach and in rats treated for at least 3 days. The reactive deposits are located in the cytoplasm of the upper glandular cells and in the lumen of the antral glands. These results suggest that aluminium is absorbed through the antral mucosa and may be re-excreted through the glandular mucus flow into the digestive lumen where it will be absorbed again. We hypothesize that the metal could act as a delayed-effect drug.

Administration, Oral↗
PubMed1992

[Changes in gastrointestinal mucins caused by attapulgite. Experimental study in rats].

A histochemical study was carried out to evaluate the changes occurring in mucins secreted by the rat stomach and intestine following a 7 day-treatment with a cytoprotective clay: attapulgite. Staining of gastrointestinal sections was performed with periodic acid-Schiff reagent, alcian blue pH 2.5 and pH 1.0, and with lectin conjugated with horseradish peroxidase for detecting complex carbohydrates. When compared with controls, attapulgite induced an increase in carboxylic mucin content in the cells of the crypts associated with a decrease in sulphated mucins and in binding with soy bean agglutinin in surface epithelial cells in the fundic zone. In the antrum, staining with wheat germ agglutinin was decreased in the crypt cells while Ulex europaeus agglutinin affinity was increased in the glandular cells. The duodenum was characterized by increased binding with Ulex europaeus agglutinin in Brunner's glands. These results show that the polysaccharidic components of the gastrointestinal glycoproteins are modified by attapulgite, and this mechanism may be involved in its cytoprotective effects.

Acetylglucosamine↗
PubMed1991

Galanin induces contraction of isolated cells from circular muscle layer of pig ileum.

The effects of galanin and its interaction with cholecystokinin and acetylcholine on smooth muscle cells were studied in vitro on isolated cells obtained from pig ileum circular muscle layer. Galanin induced a concentration-dependent cell contraction with a maximal contraction (24.5% decrease in cell length from control) obtained at 1 nM. The concentration of galanin inducing a half-maximal contraction was 3 pM. Tetrodotoxin (10 microM) failed to inhibit cell contraction induced by galanin (1 nM), pentagastrin (10 nM) and acetylcholine (1 microM). Atropine abolished the contraction induced by acetylcholine (1 microM), but had no effect on galanin- and pentagastrin-induced contraction. L 364,718 inhibited the contraction induced by CCK8 but not the galanin-induced contraction. At the uneffective concentration of 10 fM, galanin had a synergistic effect with an uneffective concentration of CCK8 (1 pM). These results suggest that (i) galanin contracts smooth muscle cells from pig ileum by acting on a specific receptor; (ii) galanin and either CCK or acetylcholine may act in a synergistic way to induce cell contraction.

Acetylcholine↗
PubMed1991

Involvement of 5-hydroxytryptamine in the intestinal motor disturbances induced by mast cell degranulation in rats.

Fasted rats with chronically implanted electrodes were used for investigation of the effects of mast cell degranulation induced by compound 48/80 and BrX-537A and their antagonism by previous administration of 5-hydroxytryptamine (5-HT) antagonists on duodenal and jejunal myoelectric activity. Administered i.p., both 48/80 (1 mg/kg i.p.) and BrX-537A (2 mg/kg i.p.) abolished the intestinal spiking activity of duodeno-jejunum with a progressive recovery, BrX-537A being less active. These effects were dose-related. Injected prior to 48/80, methysergide (1 mg/kg) reduced by about 80% both duodenal and jejunal inhibition of spiking activity with early recovery of a normal pattern. In contrast, ketanserin (1 mg/kg) had selective reducing effects on the duration of the spiking inhibition induced by 48/80 and BrX-537A on the duodenum only. Zacopride (1 mg/kg) and ICS 205-930 (50 micrograms/kg) shortened and suppressed, respectively, the inhibition of intestinal spiking activity with early restoration of intestinal motility in both duodenum and jejunum. We conclude that, in fasted rats (i) the degranulation of peritoneal mast cells induces alterations in intestinal myoelectric activity through the release of 5-HT (ii) these effects are mainly mediated through both 5-HT1 and 5-HT3 receptors.

Animals↗
PubMed1991

Central and peripheral control of postprandial pyloric motility by endogenous opiates and cholecystokinin in dogs.

The role of endogenous opiates and cholecystokinin (CCK) in the control of postprandial pyloric myoelectric activity was investigated in conscious dogs with chronically implanted intraparietal electrodes at the gastroduodenal junction. Meals consisted of either 20 g/kg of canned food (standard meal) or the same food supplemented with 0.5 mL/kg of arachis oil (fat meal). During the 6 hours after standard and fat meals, the number of pyloric spike bursts, 2-4 seconds in duration, was 61.8 +/- 15.8 and 49.9 +/- 12.7/15 minutes, respectively. Administered 15 minutes before a fat meal, naloxone (50 micrograms/kg IV) decreased the number of spike bursts by 31.4%, whereas methyl-levallorphan, a peripheral opiate antagonist, increased postprandial spike activity by 22.2% when administered IV (0.5 mg/kg) and decreased it when administered intracerobroventricularly at a dose of 10 micrograms/kg. These two antagonists administered in the same conditions before a standard meal had no effect on the postprandial spike activity. A 1-hour infusion of cholecystokinin octapeptide (CCK-8), 500 ng.kg-1.h-1 IV and 50 ng.kg-1.h-1 intracerebroventricularly, performed 1 hour after a standard meal induced a 19.6% and 15.8% decrease in the number of pyloric spike bursts, respectively. Both naloxone IV (50 micrograms/kg) and methyl-levallorphan intracerebroventricularly (10 micrograms/kg) administered before the infusion of CCK-8 reinforced this pyloric inhibition, which was antagonized by methyl-levallorphan IV (0.5 mg/kg). The CCK antagonist asperlicin, 200 micrograms/kg IV and 20 micrograms/kg intracerebroventricularly, administered before a fat meal increased pyloric spike bursts by 22.0% and 31.5%, respectively. These results indicate that after a fat meal, endogenous opiates exert a peripheral inhibitory and central stimulatory control of pyloric motility; they suggest the involvement of both peripheral and central release of CCK.

Animals↗