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Biomedical subjects

J Fioramonti

Publications and source records attributed to J Fioramonti.

At least 127 records · Page 7Linked to original sources
PubMed1991

Action of endogenous prostaglandins on postprandial pyloric motility: a possible modulation by fats.

The involvement of endogenous prostaglandins (PGs) and the effect of exogenous PGs on the myoelectrical activity of the pylorus were examined for 6 hours after a meal in dogs chronically fitted with intraparietal electrodes on the gastroduodenal junction. The animals received either a standard meal or a fat meal which consisted of canned food added or not (standard meal) with arachis oil. The cyclooxygenase inhibitors, indomethacin (1 mg/kg) and piroxicam (0.2 mg/kg) given prior a fat meal significantly increased the frequency of pyloric spike bursts but did not modify the pyloric motility associated with a standard meal. Synthetic derivatives of PGE1 (misoprostol, 5-10 micrograms/kg) or PGE2 (enprostil 0.5-1 micrograms/kg) reduced the frequency of pyloric contractions after a fat but not a standard meal. It is suggested that both endogenous and exogenous prostaglandins may modulate postprandial pyloric motility when fats are present in sufficient amount into the meal.

Administration, Oral↗
PubMed1991

Absorptive and motor components of the antidiarrhoeal action of loperamide: an in vivo study in pigs.

The effects of loperamide (0.1 mg/kg orally) on net colonic water absorption, orocolonic transit time, and intestinal motility were investigated in pigs chronically fitted either with two cannulas in the proximal colon and a catheter in the duodenum and the ileum or with intraparietal electrodes on the duodenum, jejunum, caecum, and proximal colon and a duodenal catheter. Loperamide, given 20 minutes before a meal reduced significantly colonic net water absorption for 10 hours after eating. It also reduced colonic flow rate, increased orocolonic transit time, modified the postprandial intestinal motility by inducing supplementary phase 3 motor complexes and did not affect caecocolonic motility. Intraduodenal infusion of a hypertonic solution of mannitol (900 mOsm/l; 0.6 ml/minute) for the first postprandial hour strongly reduced or reversed net colonic water absorption, increased the colonic flow rate, accelerated the orocolonic transit, and induced profuse diarrhoea. After loperamide administration, all these effects were blocked and the relative colonic water absorption, expressed as the fraction of flow entering the colon, was strongly increased. Mannitol did not modify motility of the small and large intestine, and supplementary phase 3 motor complexes were observed when mannitol infusion was preceded by loperamide administration. It is concluded that in experimental osmotic diarrhoea loperamide causes a reduction in digesta flow entering into the colon, mediated by its action on small intestinal motility, and an increase in colonic water absorption.

Animals↗
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↗
PubMed1990

Selective stimulation of colonic motor response to a meal by sigma ligands in dogs.

The influence of central vs. peripheral administration of sigma ligands (dl- and l-N-allylnormetazocine, 1-3-di-o-tolylguanidine, (+) cinnamyl-1-phenyl-1-N-methyl-N-cyclopropylene and phencyclidine on colonic motility was investigated in fasted and fed dogs equipped with strain-guage transducers implanted on proximal and transverse colon. When injected intravenously at a dose of 0.25 mg/kg just before feeding, dl- or d-N-allylnormetazocine, 1-3-di-o-tolylguanidine, and (+) cinnamyl-1-phenyl-1-N-methyl-N-cyclopropylene (but not phencyclidine) enhanced the colonic motor response to a meal by increasing the 0-4-hour motility indexes from 64.1%-159.3% in both the proximal and transverse colon but had no effect on colonic motility in fasted animals or animals injected intracerebroventricularly. The motor-stimulatory effects of d-N-allylnormetazocine (1 mg/kg), 1-3-di-o-tolylguanidine (0.25 mg/kg), and (+) cinnamyl-1-phenyl-1-N-methyl-N-cyclopropylene (1 mg/kg) were abolished after previous treatment with haloperidol (0.5 mg/kg, intravenous) but not after sulpiride (0.1 mg/kg) or (+) R-(+)-8-chloro-2,3,4,5-tetrahydro-3- methyl-5-phenyl-1-H-3-benzozepine-OH. Prazosin (0.1 mg/kg, intravenous) and 1-methyl-3-(2-indolyl)amino-5-phenyl-3H-1,4-benzodiazepin-2-one (0.01 mg/kg) also suppressed the enhancement of the colonic motor response to eating induced by d-N-allylnormetazocine, 1-3-di-o-tolylguanidine, and (+)cinnamyl-1-phenyl-1-N-methyl-N-cyclopropylene whereas naltrexone did not affect their effects. It is concluded that d-N-allylnormetazocine, 1-3-di-o-tolylguanidine, and (+)cinnamyl-1-phenyl-1-N-methyl-N-cyclopropylene stimulate the postprandial colonic motility in dogs by acting selectively on sigma receptors located peripherally and probably by affecting the release of cholecystokinin octapeptide through a central adrenergic mechanism.

Animals↗
PubMed1990

[Colonic motility in the irritable bowel syndrome].

The importance of colonic motor disorders during the irritable bowel syndrome is recognized, but, paradoxically, their description has yet to be perfected. Among the fundamental questions that remain unanswered, three are of prime importance: a) are there one or more specific disturbances in basal colonic motility? b) can specific motor disorders be induced by certain situations, for instance, during stress? c) is there any real relationship between clinical symptoms and coexisting motor disorders? The answers to these questions are full of ambiguities; this may be explained by the difficulty with which methods of investigation are performed as well as the heterogeneous character of the disorders. Presently, recording colonic myoelectric activity over a 24 hour period or more might prove to be useful in increasing our knowledge on motor disorders. It is not at all certain that a specific basal abnormality exists and the results of the effects of stress vary according to the methods used. Segmental hyperactivity in painful constipation, abnormal colonic response to alimentation in the case of painful bloating, and propulsive hyperactivity with absence or decrease in the "sigmoid brake" during painless diarrhea have been noted on basal motor activity recordings during sleep and after meals. Myoelectric disorders, however, are seen in only two-thirds of patients with intestinal functional disorders. "Sensitivity", personality, or other disorders, and particularly, intestinal disorders, can contribute to explain the pathophysiology of "irritable bowels" in which the role of colonic disorders has yet to be shown.

Action Potentials↗
PubMed1989

[Role of motility in intestinal transit and absorption].

The relationships between small intestinal motility, transit of digestive content and absorption of nutrients have been examined at two levels: intestinal contraction and motor profile mainly characterized by the cyclic occurrence of migrating motor complexes (MMC). The propulsive efficacy of a contraction depends upon several parameters such as amplitude, orientation, distance of propagation, and is modulated by the nature and the amount of digestive contents. The most rapid transit and the highest flow of digesta appear during the postprandial state and the phase 2 of MMC. Both contractions and MMC are correlated with increases in transmucosal potential difference which corresponds in part to the ionic permeability of the mucosa. Using analogic models or anesthetized animals, it has been shown that intestinal contractions are associated with water absorption. Simultaneous measurements of duodenal motility and glycemia in awake animals indicate that glucose absorption mainly occurs during periods of activity of the MMC and is minimum during the phases of quiescence. Such relations have also been determined between intestinal motility and arterial blood flow, but then are dependent upon the presence of nutrients or bile in the intestinal lumen. Finally, the complexity of the relationships between motility, transit and absorption is mainly due to the numerous parameters which characterize an intestinal contraction and to the nature of the intestinal contents.

Animals↗
PubMed1989

[Hormonal control of intestinal motility].

There is increasing evidence that digestive hormones are involved in the regulation of the gastrointestinal motor profile in man. A typical profile of postprandial activity corresponding to the continuous occurrence of irregular contractions propagated over short distance is accompanied by an increase in plasma level of 8 to 10 identified digestive hormones. Four of them (insulin, gastrin, neurotensin and CCK8) infused systemically may produce or prolong this typical "fed" pattern suggesting that they may be involved physiologically in the initiation and duration of the fed pattern. The fasted state is characterized by the cyclic occurrence of gastrointestinal migrating motor complexes (MMC) which are associated with cyclic changes in plasma levels of motilin, somatostatin pancreatic polypeptide and gastrin. Numerous recent findings support the hypothesis that an increase in motilin initiates the MMC at foregut level which, in turn, produces the release of somatostatin. These hormones may be responsible for the aboral migration of MMC from the duodenum to the ileum and for the cycling rhythm by affecting blood levels of motilin (and/or) pancreatic polypeptide.

Animals↗
PubMed1989

Effects of sennosides on colonic myoelectrical activity in man.

The effects of sennosides on colonic myoelectrical activity were investigated in man. Spiking activity of the left and sigmoid colons was continuously recorded in seven constipated patients during two sessions from 5:00 PM to 9:00 AM. Each patient received orally at 7:00 PM on two consecutive days 30 mg of sennosides one day (sequence S) and placebo on the other (sequence P) in a random fashion. A significant (P less than 0.05) increase of peristaltic activity (migrating long spike bursts or MLSBs) after sennosides was observed between 1:00 and 7:00 AM, and a corresponding decrease between 7:00 and 9:00 AM. No change was noted in total short spike burst (SSB) activity or in SSBs characteristic of the rectosigmoid area. This study indicates that the main modification of colonic motility induced by sennosides was a stimulation of propulsive activity (MLSBs), which occurred between 6-12 hr after oral administration, the delay required for orocecal transit and metabolism of the drug.

Action Potentials↗
PubMed1989

Rectal potential differences in irritable bowel syndrome and in inflammatory bowel diseases in man.

We have studied rectal potential difference (pd) in 200 subjects: 30 healthy volunteers or control patients, 46 patients with irritable bowel syndrome (IBS) and painless diarrhoea (group I), 60 IBS patients without diarrhoea (group II) and 64 patients with inflammatory bowel disease (IBD) with (group III, n = 41) or without (group IV, n = 23) rectal involvement. Pd measurement used a rectal perfused probe and a subcutaneous needle both connected, via agar-KCl bridges, to calomel electrodes and a millivoltmeter. Statistical analysis used Student's t-test for paired and unpaired data and Mann-Whitney U-test as appropriate. Mean rectal pd values were, respectively -43.5 +/- 8.7 mV in control group, -32.9 +/- 10.2 mV in IBS-group I patients (P less than 0.001), -41.3 +/- 12 mV in IBS-group II patients (NS), -21.4 +/- 14.1 mV in IBD patients with rectal involvement (P less than 0.001), and -45.1 +/- 14.3 mV in IBD-group IV patients (NS). A histological examination was performed in 36 IBS patients; mean rectal pd was significantly decreased in patients showing abnormal patterns (n = 27, pd = -31.8 +/- 9 mV) compared to patients with normal mucosa (n = 9, pd = -41.1 +/- 6.5 mV; P less than 0.01). These results show that: (1) potential difference is significantly decreased in patients with ulcerative and rectal involvement; (2) in patients with Crohn's disease, normal rectal pd values do not assess the appearance of colonic mucosa above; (3) patients with IBS and diarrhoea also present a significant diminution in mean rectal pd. Although the mechanisms involved remain unclear, rectal pd measurement appears to be an objective test for intestinal mucosae weakness in functional or inflammatory diseases of the large intestine and rectum.

Adult↗
PubMed1989

Central and peripheral beta-adrenergic influences on reticulo-rumen and upper-gut myoelectrical activity in sheep.

The effects of intravenous (i.v.) and intracerebroventricular (i.c.v.) administration of beta-adrenoceptor agonists were evaluated on the reticulo-rumen and upper-gut myoelectrical activity in six ewes chronically fitted with intraparietal electrodes and a cannula in a lateral ventricle of the brain. Intravenous infusion of the beta 1 agonist dobutamine (30 micrograms/kg/min for 15 min) reduced the frequency of reticulo-ruminal and abomasal contractions and stimulated duodeno-jejunal motility, inducing a Phase III on the jejunum. These effects were reproduced by i.c.v. dobutamine at a dose of 10 micrograms/kg. Intravenous infusion of the beta 2 agonist ritodrine (15 micrograms/kg/min for 15 min) selectively inhibited antral and duodenal motility. Ritodrine i.c.v. (15 micrograms/kg) did not affect forestomach or gastrointestinal motility. The mixed beta 1, beta 2 agonist isoprenaline infused i.v. (0.6 micrograms/kg/min for 15 min) reproduced the effects of i.v. dobutamine, except at the antro-duodenal level which was strongly inhibited. The effects of i.v. dobutamine were antagonized by i.v. or i.c.v. acebutolol, a specific beta 1 antagonist. The effects of i.v. ritodrine were blocked by i.v. but not i.c.v. administration of propranolol, a mixed beta 1, beta 2 antagonist. These data indicate that the stimulation of central beta 1 adrenoceptors inhibits forestomach and antral motility and stimulates duodeno-jejunal motility. Stimulation of peripheral beta 2 adrenoceptors selectively inhibits duodeno-jejunal motility.

Acebutolol↗
PubMed1989

Involvement of different receptors in the central and peripheral effects of histamine on intestinal motility in the rat.

The effects of histamine on intestinal motility have been investigated in conscious rats, fed or fasted, using an electromyographic method. Histamine peripherally administered (10 mg kg-1) in 15 h fasted rats induced an inhibition followed by a period of irregular spiking activity disrupting the duodenojejunal migrating myoelectric complexes (MMC) and suppressed the postprandial motor spiking activity when administered 50 min after a meal. The selective agonist of the H1-receptors, 2-pyridylethylamine (2-PEA) induced an irregular spiking activity while dimaprit acting on H2-receptors, inhibited the MMC pattern. Effects of peripherally administered histamine were antagonized by previous administration of chlorpheniramine (0.5 mg kg-1 i.p.) and in a lesser extent by cimetidine (10 mg kg-1 i.p.). Histamine (1-10 micrograms) administered intracerebroventricularly (i.c.v.) in fasted rats increased the motor cycle frequency and immediately restored the MMC pattern when given to fed rats. Among the three agonists of the H1- H2- and H3-receptors (2-PEA, dimaprit and R-alpha-methylhistamine, respectively) only R-alpha-methylhistamine (1-10 micrograms i.c.v.) was able to reproduce this effect. It is concluded that the effects of histamine on intestinal motility were centrally and peripherally mediated involving mainly H1-receptors at the peripheral level and H3-receptors at the CNS level.

Animals↗
PubMed1989

Water absorption from the pig proximal colon: relations with feeding and flow of digesta.

Net water absorption from the proximal colon was determined at 2 h intervals for 10 h after a meal in four pigs chronically fitted with two cannulas in the proximal colon (1st and 2nd coil) and a catheter in the ileum. Water flux was measured by infusing a marker (51Cr-EDTA) at a constant rate into the ileum and by sampling colonic content through the cannulas. Two hours after the meal water was absorbed by the colonic segment situated between the two cannulas at a rate of 0.7 +/- 0.1 ml/min. Then the net water absorption increased progressively and reached a maximum (1.7 +/- 0.3 ml/min) 8 h after eating. These postprandial changes in water absorption were positively correlated (r = 0.63, n = 40) with changes in the flow of digesta at the level of the proximal cannula. The concentration of volatile fatty acids and the osmolality of the digesta, as well as the transit time of a marker (phenolsulphonphthalein) between the two cannulas, did not significantly fluctuate after the meal and were not correlated with water absorption. Antibiotic treatment for 3 days (neomycin, 15 g/day, continuously infused into the ileum) induced a 90% decrease in volatile fatty acid concentration but did not modify colonic water absorption nor its postprandial changes. These results show a postprandial pattern of colonic water absorption which is mainly controlled by the flow of digesta into the colon.

Animals↗
PubMed1989

Involvement of different mechanisms in the stimulatory effects of cholecystokinin octapeptide on gastrointestinal and colonic motility in dogs.

The effects of an intravenous infusion of cholecystokinin octapeptide (CCK-8, 1 microgram.kg-1.h-1) were investigated in conscious fasted dogs chronically fitted with strain-gauge transducers on the antrum, the jejunum, and the colon. Attempts to antagonize the increase of motility appearing at the three levels during CCK infusion were made using different blockers to elucidate the mechanisms involved. Asperlicin (a specific CCK antagonist) blocked the effects of CCK-8 at the three levels, while atropine and somatostatin were only effective in the jejunum and colon. Methyl-levallorphan (a mu-opiate antagonist that poorly crosses the blood-brain barrier) antagonized the CCK-induced colonic stimulation when intracerebroventricularly administered. Serotonin, histamine, substance P, and K-antagonists as well as a benzodiazepine did not modify the CCK-8 induced stimulation. It was concluded that the stimulatory effect of CCK-8 resulted from (a) a direct stimulation of the smooth muscle cells at gastric level, (b) a cholinergic activation of the jejunum and the colon, and (c) the involvement of a mu-opioid central component in the colonic response only.

Animals↗
PubMed1989

Vagally mediated inhibition of acoustic stress-induced cortisol release by orally administered kappa-opioid substances in dogs.

The effects of oral vs. iv administration of kappa- and mu-opioid agonists on plasma cortisol release induced by acoustic stress (AS) were evaluated in fasted dogs with an implanted jugular catheter. AS was induced by 1 h of music (less than or equal to 86 decibels) played through earphones and was accompanied by a 382% maximal rise in plasma cortisol after 15-30 min. Administered orally 30 min before the AS session, both U-50488 (0.1 mg/kg) and PD 117-302 (0.05 mg/kg) significantly (P less than or equal to 0.01) decreased (by 71.2% and 80.9%, respectively) the maximal increase in plasma cortisol induced by AS, while bremazocine, morphine, as well as iv administration of U-50488 at similar doses were ineffective. The effects of U-50488 and PD 117-302 orally administered (0.1 mg/kg) on the hypercortisolemia induced by AS were abolished by pretreatment with iv naloxone (0.1 mg/kg) or MR 2266 (0.1 mg/kg). Naloxone given alone significantly (P less than 0.01) increased basal plasma cortisol, without affecting cortisol increase induced by AS. Vagotomy abolished the effects of orally administered U-50488 on the AS-induced increase in plasma cortisol. Neither U-50488 nor PD 117302 (0.1 mg/kg, orally) reduced the increase in plasma cortisol induced by intracerebroventricular administration of ovine CRF (100 ng/kg). It is concluded that kappa- but not mu-opioid agonists are able to inhibit the stimulation of the hypothalamo-pituitary-adrenocortical axis induced by AS by acting selectively on peripheral kappa-receptors located in the wall of the proximal gut. This action is neurally mediated through afferent vagal fibers affecting central nervous system release of CRF induced by a centrally acting stressor.

Administration, Oral↗
PubMed1989

[Effects of corticoids, 5-aminosalycilic acid and sucralfate on the potential difference of the rectum in inflammatory colitis in man].

Glucocorticoids are able to increase ionic transport across the rectal mucosa and improve the potential difference (PD) which is known to be decreased in inflammatory bowel diseases in man. The aim of this study was to evaluate the effects of therapeutic enemas or parenteral drugs used in the treatment of inflammatory colitis, by means of rectal PD variations. Seventeen patients (10 women, 7 men, mean age 47 +/- 16 years) with chronic colitis and rectal involvement were studied (ulcerative colitis: n = 12, Crohn's disease n = 4, radiation proctocolitis : n = 1). In each patient, mean PD basal value was measured before treatment for 30 min; a few days later PD measurements were performed 5 h after either intravenous administration of hydrocortisone (HC i.v.: 100 mg) or local administration of therapeutic enemas: 5-aminosalicylate acid (5-ASA: 4 g), hydrocortisone (HC L: 100 mg) or sucralfate (S: 1 g). Statistical analysis used Student's T test for paired or unpaired data, the Mann-Whitney U or Wilcoxon test. PD increased from: - 30.7 mV to - 45.6 mV after HC i.v. (p less than 0.001), - 31.8 mV to - 48.7 mV after HC L (p = 0.01), - 29.8 mV to - 39.8 mV after 5-ASA (p less than 0.01) and - 20.6 mV to - 24.9 mV after sucralfate (NS) respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗