[Management of endometriomas in France: A survey of practices]. / Prise en charge des endométriomes en France : enquête de pratiques.

OBJECTIVES: To present an overview of French practices for the management of endometriomas. METHODS: We carried out a nationwide survey of practices concerning the management of endometriomas between October 2021 and January 2022. This study was carried out by means of two questionnaires sent to surgical centers used to treat endometriosis (n=62) and to Assisted Reproductive Technology (ART) centers (n=102). RESULTS: At the end of the survey, 39/62 (62.9%) surgical teams from the centers contacted had given a response and 51/102 (50.0%) from ART centers. Laparoscopic cystectomy was the technique most frequently used by almost two thirds of the surgical teams (61%) when there was no known infertility, whereas it was the most common technique for only 14% of the ART teams. On the contrary, ultrasound-guided sclerotherapy was the most frequent technique for more than half of the ART teams (56%) and for only 8% of the surgical teams. In case of recurrence, 49% of surgical teams would choose ultrasound-guided sclerotherapy. Prior to IVF, 73% of ARP teams stated that they 'rarely' treated endometriomas. CONCLUSION: The results of our study show a certain variability in practices between different centers and depending on the presence or absence of infertility for the management of endometriomas in France.

Local treatment of pressure sores in the elderly: amino acid copolymer membrane versus hydrocolloid dressing.

OBJECTIVE: To compare the clinical effectiveness and wound management properties of a copolymer membrane, Inerpan (Synthélabo), and a hydrocolloid dressing, Comfeel (Coloplast), in the treatment of decubitus ulcers in the elderly. DESIGN: Open, randomized, multicentric French study, with two parallel groups of patients. PATIENTS: 168 in-patients aged more 65 years (mean age: 82 years) suffering from grade II to grade IV (in the Shea classification) pressure sores. TRIAL PERIOD: Either 8 weeks or until the ulcer healed, whichever occurred first. MEASUREMENTS: In addition to a complete physical examination, patients were evaluated at baseline for nutritional status and risk factors. The wounds were described, their depth scored, and the areas traced at Weeks 0, 1, 2, 4, 6, and 8. The number of dressings used was recorded. RESULTS: Thirty-one Inerpan-treated patients and 23 Comfeel-treated patients achieved healing (P = 0.089), with respective median healing times of 32 and 38 days. Healing times were compared using survival curves (in the whole population) adjusted for ulcer depth effect and showed a significant difference in favor of Inerpan (P = 0.044 and 0.014). Progress of healing (percentage of ulcer healed) was calculated in the two groups. Clinically assessed the treatment performance scored at the completion of the study showed better results with Inerpan (P < 0.05). Both groups were similar in terms of granulation/exudation scores, surrounding skin, and ease of care. CONCLUSION: It is concluded that Inerpan is easy to use, safeguards the healing process, and is of particular value in the management of pressure sores.

Effects of fedotozine on gastrointestinal motility in dogs: mechanism of action and related pharmacokinetics.

The effects of fedotozine, (+)-(1R)-1-phenyl-1-[(3,4,5-trimethoxy)benzyloxymethyl]-N,N-dim eth yl- n-propylamine, on motility of the antrum and small intestine were investigated in dog. In fasted dogs, following i.v. administration, fedotozine at 1 and 2 mg kg-1 stimulated and at 5 mg kg-1 inhibited antral motility. Between 1 to 5 mg kg-1, fedotozine exhibited a sustained and potent stimulatory effect on the small intestine inducing 1 to 4 phases III of the migrating motor complex (MMC) lasting up to 32 min in the duodenum and migrating to the jejunum. Following oral administration, fedotozine at 2.5 and 5 mg kg-1 constantly stimulated both antrum and small intestinal motility. In fed dogs, fedotozine i.v. (2 mg kg-1) increased antral motility and induced phase III of MMC in the place of postprandial pattern. Naloxone (0.3 mg kg-1 i.v.) and naloxone methylbromide (2 mg kg-1 i.v.) inhibited the stimulatory effects of fedotozine on gastrointestinal motility indicating a peripheral opiate site of action of the drug whereas phentolamine, hexamethonium, propranolol and methysergide were inactive. In-vitro fedotozine showed submicromolar affinity for opiate receptors with a weak specificity for the mu-receptors in guinea-pig brain and myenteric plexus preparations. Plasma concentrations in dogs receiving fedotozine administered orally at 2.5 mg kg-1 (and in all dogs except one at 5 mg kg-1) were below the detection limit (less than 20 ng g-1). In contrast, tissue concentrations in the muscle and mucosal layers of the gut were above 1 microgram g-1.(ABSTRACT TRUNCATED AT 250 WORDS)

[Effects of trimebutine on intestinal motility in dogs]. / Effets de la trimébutine sur les motricités digestives chez le chien.

The effects of intravenous, oral, intracerebroventricular and local intra-arterial administration of trimebutine were investigated in dogs whose digestive tract had been fitted with electrodes and strain gauge transducers. In fasted conscious dogs, trimebutine (5 mg/kg) stimulated small bowel motility with induction of a propagated phase of regular spiking activity. This stimulation was associated with weak inhibition of gastric motility and a biphasic response of the colon characterized by stimulation followed by inhibition. By the oral route, trimebutine (20 mg/kg) stimulated gastrointestinal motility. The duration of the intestinal migrating phase 2 was increased whereas an additional migrating phase 3 developed. These effects were associated with an increase in colonic contractions lasting two hours. The stimulating effect of trimebutine (phase 3) on intestinal motility was not reproduced after intracerebroventricular administration and was abolished by previous intravenous, but not intraventricular, administration of naloxone. The local effects of trimebutine on the circular muscle of canine gastrointestinal tract were studied after close intra-arterial injection in anesthetized dogs. Under these conditions, the drug stimulated the resting gut through its neural and direct smooth muscle components while it inhibited the contractions induced by field stimulation. In conclusion, the excitatory effect of trimebutine seems to be mediated by mu or delta receptors while its inhibitory activity might involve kappa opiate receptors.

Opposite effects of kappa-opioid agonists on gastric emptying of liquids and solids in dogs.

The influence of oral (p.o.) administration of kappa-(U-50488, tifluadom) and mu- (morphine, DAGO) opioid substances on gastric emptying of liquids and solids in a standard canned dog food meal was evaluated using a double-radiolabeled technique in dogs fitted with gastric cannulas. One hour after feeding, 28.6% +/- 3.6% (mean +/- SD) of the solid phase and 27.1% +/- 8.6% of the liquid phase of the meal had been emptied. Both U-50488 and tifluadom given orally (0.01-0.1 mg/kg) significantly increased (p less than 0.05) the 1-h emptying of the solid phase of the meal by 23.1%-49.6%. In contrast, both drugs significantly reduced emptying of liquids. These effects were not reproduced when similar doses were given intravenously. Oral administration of morphine or DAGO (0.01-0.1 mg/kg) did not affect gastric emptying, whereas an inhibited emptying of solids was observed for morphine at a higher dose (1 mg/kg p.o.). At a dose of 100 micrograms/kg i.v. both naloxone and MR 2266 (0.1 mg/kg) abolished the effects of orally administered U-50488 on gastric emptying of solids and liquids. It is concluded that kappa- but not mu-agonists act locally to alter gastric emptying of a standard meal in dogs, having opposite effects on solid and liquid phases. A selective local stimulation of kappa mucosal or submucosal receptors of the gastroduodenal area may explain such effects.

CNS blockade of acoustic stress-induced gastric motor inhibition by kappa-opiate agonists in dogs.

The influence of the kappa-opioid substances dynorphin-(1-13), ethylketocyclazocine (EKC), and U 50488 and mu-opioid substance [D-Ala2-N-Me, p-nitro-Phe4-Gly5-ol]enkephalin (DAGO) on gastric motor inhibition induced by acoustic stress (AS) was investigated in fasted dogs with strain-gauge transducers chronically implanted on the antrum and proximal jejunum. AS induced by 1 h of music (80-90 dB) was delivered through earphones. Starting 40-50 min after the last migrating motor complex (MMC), AS delayed by 114% the occurrence of the next gastric MMC, whereas intestinal motility was unaffected. During AS plasma cortisol increased (P less than 0.05) by 215%, 15 min after the beginning of noise and reached a peak at 30 min. When administered intracerebroventricularly at doses higher than 20 ng/kg, dynorphin abolished the AS-induced lengthening of the gastric MMC cycle. Similar blockade was observed for EKC and U 50488 at doses of 10 and/or 20 ng/kg, but DAGO was unable to affect the AS-induced gastric inhibition at any dosage tested (20-200 ng/kg icv). At doses effective against AS-induced hypomotility, both dynorphin-(1-13) and EKC reduced significantly (P less than or equal to 0.05) the associated maximal increase in plasma cortisol level. Plasma cortisol was unmodified by intracerebroventricular administration of DAGO. None of the agonists affected basal plasma cortisol levels or the increase (0-90 min) in response to intravenous adrenocorticotropic hormone (ACTH, 5 IU). Both EKC (50 ng/kg) and U 50488 (20 ng/kg) were unable to antagonize the inhibitory effect of ovine corticotropin-releasing factor (CRF, 100 ng/kg icv).(ABSTRACT TRUNCATED AT 250 WORDS)

Peripheral antagonistic action of trimebutine and kappa opioid substances on acoustic stress-induced gastric motor inhibition in dogs.

The effects of intracerebroventricular (i.c.v.), intravenous (i.v.) and oral (p.o.) administration of trimebutine on the gastric motor inhibition induced by acoustic stress were investigated in fasted dogs fitted with strain-gauge transducers on the antrum and proximal jejunum. Started 40-50 min after the last migrating motor complex, a 1 h acoustic stress delayed by 111% the occurrence of the next gastric migrating motor complex without affecting the jejunal motor pattern. This inhibition of gastric migrating motor complex induced by acoustic stress was abolished by previous p.o. administration of trimebutine (1 mg/kg) but not by its i.v. (0.1 mg/kg) or i.c.v. (0.01 mg/kg) injection. The trimebutine blockade of gastric motor alterations induced by acoustic stress was suppressed after previous i.v. treatment with MR 2266 (0.3 mg/kg) but was unaffected by naloxone (0.3 mg/kg). Furthermore oral administration of U-50488H (10 micrograms/kg) and ethylketocyclazocine (10 micrograms/kg) respectively abolished and reduced the acoustic stress-induced delay of the occurrence of the gastric migrating motor complex. We concluded that trimebutine is able to antagonize the gastric motor disturbances induced in dogs by acoustic stress, probably by acting selectively on peripheral kappa receptors located in the wall of the proximal gut and directly stimulated from a mucosal site.

Effects of orally vs. parenterally administrated trimebutine on gastrointestinal and colonic motility in dogs.

The influence of oral administration and intravenous infusion of trimebutine maleate (TMB) and N-desmethyl TMB (NDTMB), its main metabolite, was investigated in conscious dogs equipped with chronically implanted strain-gauges. In fasted dogs, TMB (10 to 20 mg/kg per os) delayed the occurrence of the next activity front on both stomach and duodenum by reinforcing the duration of the intestinal phase II. It also induced the occurrence of an additional migrating phase III. These effects were associated with a colonic stimulation generally followed by an inhibition. Comparatively NDTMB at similar dosages disrupted the antral cyclic phases which were replaced by continuous low amplitude contractions during 5-7 h. The MMC pattern persisted with a significant increase in the duration of phase II, and the colonic motility was inhibited during 4.3 to 6.7 h. Infused intravenously at a dose of 3 mg X kg-1 X h-1, TMB immediately inhibited the gastric cyclic contractions in fasted dogs. As for the oral route, the small bowel exhibited an increase in the duration of phase II frequently associated with the occurrence of an additional phase III. Furthermore an inhibition of the colonic motility was observed only at the end of the infusion and lasted at least 4 h. At similar dosage NDTMB had less pronounced inhibitory effects on gastric activity fronts and in contrast with TMB, the inhibitory effect on the colonic motility was observed as soon as the infusion of NDTMB started. These data demonstrate that orally administered TMB stimulates intestinal motility as previously described for i.v. route but in contrast to parenteral administration also stimulates antral and colonic motility.(ABSTRACT TRUNCATED AT 250 WORDS)

[Effect of trimebutine on the plasma postprandial release of gastrointestinal hormones in the dog]. / Effet de la trimébutine sur la libération plasmatique postprandiale d'hormones gastrointestinales chez le chien.

The injection of trimebutine induces in the dog an increase of plasma motilin during the fasting period as well as after a meal. We studied the effect of trimebutine on several gastrointestinal hormones released into the circulation by the ingestion of a meal. The intravenous administration of trimebutine (10 mg/kg/h) in 4 dogs abolished the postprandial increase in plasma gastrin, pancreatic polypeptide, insulin, glucagon and GIP. Trimebutine could therefore, by its effects on various regulatory peptides, influence several digestive functions. Its mode of action could probably involves complex mechanisms, including paradoxical effects. The possibility that motilin is a mediator of the trimebutine effect on small bowel smooth muscle is discussed.

Effect of trimebutine on intestinal motility and plasma motilin in the dog.

In a previous report, trimebutine was shown to induce premature periods of phase III activity in fasting dogs, and its action was blocked by naloxone. In this study, we observed that trimebutine (5 mg X kg-1 iv) could induce premature phase IIIs in canine small intestine during interdigestive and digestive periods; trimebutine-induced phase IIIs were migrating along the small intestine faster than spontaneous activity fronts and; trimebutine-induced phase IIIs were accompanied by sharp rises in concentrations of plasma motilin. To further elucidate the trimebutine-stimulatory mechanism, we verified its effects on the release of various circulating peptides that influence intestinal motility: short-interval blood sampling during trimebutine infusion revealed that plasma motilin increases induced by trimebutine preceded the beginning of phase III in proximal duodenum; and gastrin and insulin postprandial releases were abolished by trimebutine. Therefore, trimebutine, by its simultaneous but opposite effects on various peptides that individually carry positive (e.g., motilin) or negative (e.g., gastrin and insulin) influences on the generation of activity fronts, could alter the equilibrium between stimulatory and inhibitory forces in such a way that, in some circumstances (e.g., postprandial period), stimulatory mechanisms become predominant.

Central and peripheral control of gastrointestinal and colonic motility by endogenous opiates in conscious dogs.

The effects of two enkephalin analogues, (D-Ala2, Met5) and (D-Ala2, D-Leu5) enkephalinamide, on gastrointestinal and colonic motility were investigated in conscious fasted and fed dogs using chronically implanted strain gauges. The drugs, abbreviated here with the names DALAMIDE and DADLE, respectively, were administered by using both the intracerebroventricular and intravenous routes at increasing doses. In fasted dogs when administered via the intracerebroventricular route at a dose of 20 ng X kg-1, DALAMIDE disrupted the migrating myoelectric complex pattern. A similar effect was obtained only with a dose 25 times higher (500 ng X kg-1) administered intravenously; at this dosage DALAMIDE administered intravenously also reduced the colonic motility index by 66%. When intracerebroventricularly administered in fed dogs, 2 h after a meal, DALAMIDE (20 ng X kg-1) inhibited gastric motility but restored the jejunal migrating myoelectric complex pattern as "ectopic" complexes for 4-6 h. This effect however was not reproduced by intravenous treatment even at the highest dose used (500 ng X kg-1). Both intracerebroventricular and intravenous administration of DADLE, at doses as high as 100 and 500 ng X kg-1, respectively, affected neither the motility pattern nor the motility index of the antrum and proximal jejunum in the fasted or fed state. However, intracerebroventricular, but not intravenous, administration produced a short (10-15 min) increase of colonic motility. These results suggest that (a) Met-enkephalin influences the gastrointestinal motility predominately by a central action, manifested as a migrating myoelectric complex "reorganizing" effect in fed dogs; (b) Leu-enkephalin exerts a predominately centrally mediated stimulation of colonic motility, whereas Met-enkephalin inhibits it probably by a peripheral mechanism.

Early changes in plasma pancreatic polypeptide, somatostatin, gastrin and motilin levels induced by H. contortus infection in lamb.

Plasma levels of pancreatic polypeptide (PP), somatostatin (GH-RIH), gastrin and motilin were measured during 6-7 h after oral infection with 25 000 infective (3rd stage) larvae of H. contortus in lambs or after intravenous injection of larvae or worm antigenic (Ag) extracts. A 3-fold increase in plasma gastrin was observed during the first 60 min after infection and GH-RIH increased significantly (P less than 0.01) 180 min later whereas both PP and motilin remained unchanged. An early (60 to 120 min) increase in GH-RIH and a late (5 to 7 h) increase in PP plasma levels were observed after both worm and larvae antigenic extracts whereas plasma motilin was unaffected. Plasma gastrin was significantly (P less than 0.01) increased during 3-4 h following the injection of worm but not of larvae antigenic extract. It was concluded that the immediate hypergastrinemia following H. contortus infection is not the consequence of a general immune response of the host and is probably related to the release of unknown substance(s) by the infective larvae into the abomasum or to mucosal inflammation due to a local immune response; in contrast, the increase in plasma GH-RIH levels appeared to be the result of antigenic reactions. The other hormonal changes observed after Ag injections may be the consequence rather than the reason of changes in abomasal secretory pattern.

Effects of central and peripheral administration of dopamine on pattern of intestinal motility in dogs.

The central vs peripheral effects of dopamine on the motility pattern of the small intestine were investigated by electromyography in four conscious dogs, chronically fitted with transparietal duodenal and jejunal electrodes. In the fasted dog intracerebroventricular administration of dopamine (10 micrograms/kg) increased the duration of the interval between two consecutive migrating myoelectric complexes (MMC) while the intravenous administration at a 10-fold higher dose induced in 37.5% of trials a phase of regular spiking activity propagated over the duodenum and the jejunum. When dopamine was centrally administered 1 hr before a daily meal, the duration of the postprandial disruption of the MMC pattern was significantly (P less than 0.01) reduced from 9.4 +/- 1.8 to 3.2 +/- 1.3 hr at the level of the duodenum. Peripheral administration of dopamine did not modify the duration of the postprandial disruption. All of the central and peripheral effects persisted after vagotomy. It is concluded that in the dog dopamine acts centrally to modify the food-induced disruption of the MMC pattern and the frequency of the interdigestive myoelectric complexes.

Effects of ranitidine and oxmetidine on gastrointestinal motility in conscious dog.

Two histamine H2-receptor antagonists ranitidine and oxmetidine were tested for their effects on gastrointestinal motility in conscious fasted dogs chronically fitted with intraparietal electrodes on the antrum, duodenum and jejunum. Intravenous administration of ranitidine (3 mg/kg) stimulated gastrointestinal spiking activity through a cholinergic mechanism and increased the duration of the cycles of migrating myoelectric complexes. Oxmetidine at the same dose did not modify the gastrointestinal motor profile. These results showed clearcut differences in nonspecific effects of two H2-antagonists equipotent on gastric acid secretion.

Gastro-intestinal motor disturbances induced by lysine-acetylsalicylate treatment in sheep.

The effects of intravenous (i.v.), intramuscular (i.m.) and oral administration of lysine-acetylsalicylate (Lys-ASA) on gastro-intestinal motility were investigated in sheep using electromyography. A dose of 20 mg/kg Lys-ASA intravenously reduced the frequency of reticular contractions for 86 +/- 18 min, produced abomasal hypomotility and caused a disruption of the cyclical pattern of intestinal motility for at least 120 min. The frequency of reticular contractions measured from 20 to 30 min after Lys-ASA administration was negatively correlated (r = 0.97; P less than 0.01) to the log of the dose used for doses varying from 10 to 40 mg/kg. Similar effects were observed with intramuscular and oral dose rates of 40 and 80 mg/kg, respectively. Previous i.v. administration of phentolamine (0.1 mg/kg) or tolazoline (2 mg/kg) abolished the effects of Lys-ASA (20 mg/kg) administered intravenously on both reticular contractions and abomaso-intestinal motility. It was concluded that Lys-ASA administered at therapeutic doses in sheep produced gastro-intestinal motor disturbances and that alpha- and alpha 2-adrenergic antagonists are able to block them.

Effects of dopamine and bromocriptine on colonic motility in dog.

The effects of intravenous infusions of dopamine (0.1 to 1 mg kg-1h-1) and bromocriptine (10 to 40 micrograms kg-1h-1) on colonic motility were investigated in fasted dogs fitted with permanent strain gauges on the ascending, transverse and descending colon. Infused at rates of 0.5 and 1 mg kg-1h-1 during 1 h, dopamine immediately stimulated the motility of the descending colon; after a delay of 40 to 60 min this effect was balanced by an inhibition of the motility of the ascending and transverse colon. Bromocriptine infused intravenously at doses of 10 to 40 micrograms kg-1h-1 stimulated the motility of the whole colon but these effects were limited to the duration of the infusion (60 min). Both propranolol (0.5 mg kg-1) and tolazoline (2 mg kg-1) failed to block the effects of dopamine and bromocriptine whereas phentolamine (0.1 mg kg-1) and prazosin (0.2 mg kg-1) partially reduced the inhibitory effects of dopamine on the proximal colon. Haloperidol at doses higher than 0.2 mg kg-1 and domperidone blocked the bromocriptine-induced stimulation of colonic motility which was unaffected by previous treatment with alpha- and beta-adrenoceptor blocking agents. These results suggest that in the dog, dopamine and bromocriptine stimulate colonic motility through specific dopamine receptors. However, they suggest that the inhibitory effects of dopamine on the proximal colon which are blocked by dopamine antagonists are also partially due to an effect on alpha 1-adrenoceptors.

Evidence for central neuropeptidergic control of rumination in sheep.

Effects of intracerebroventricular (ICV) vs. intravenous (IV) administration of tetragastrin, pentagastrin, CCK8 and gastrin 17 on rumination were investigated in conscious sheep. Administered at 26 pmoles/kg ICV both tetra and pentagastrin induced a premature short (15-27 min) period of rumination only 24 +/- 7 and 23 +/- 9 min after food distribution in place of 112 +/- 44 min in controls. Similar but less pronounced effects were observed for ICV administration of an equimolar dose of gastrin 17 whereas CCK8 did not promote an early period of rumination despite its anorectic effects. Administered intravenously tetra and pentagastrin but not gastrin 17 caused early rumination only for 10 times higher doses. It is concluded that gastrin 17 and its C-terminal tetrapeptide may play a physiological role in the central control of rumination in sheep.

Proglumide: selective antagonism of the rumination but not gastric motor effects induced by pentagastrin in sheep.

The effect of intravenous (IV) vs intracerebroventricular (ICV) administrations of pentagastrin on gastro-intestinal motility and rumination were investigated by electromyography in sheep; these effects were compared to those obtained after a previous IV or ICV injection of proglumide. When ICV administered at a dose of 20 ng X kg-1, pentagastrin did not significantly affect the frequency of reticular and abomasal spiking activity but elicited a 13 to 37 min period of rumination after a delay of 23 +/- 7 min. In contrast, when IV infused at a rate of 20 ng X kg-1 X h-1 during 20 min, pentagastrin inhibited significantly the frequency of reticular and abomasal contractions for 30 to 40 min but did not induce rumination. Proglumide ICV administered (0.8 mg X kg-1) abolished the rumination induced by central injection of pentagastrin whereas a 10 times higher dose administered systemically (8 mg X kg-1 IV) did not block these effects. Both of ICV and IV administrations of proglumide at respectively 0.8 and 8 mg X kg-1 were unable to antagonize the inhibitory effects of pentagastrin on reticulum and abomasum motility. It was concluded that (i) pentagastrin acts centrally to induce rumination and that (ii) proglumide selectively blocks these effects but not the pentagastrin induced gastro-intestinal hypomotility.

Stimulatory effects of prostaglandin F2 alpha on faecal egg production in Haemonchus contortus infected sheep.

The effect of prostaglandin F2 alpha on the pattern of faecal egg count was tested in 10- to 12-month-old sheep infected with 20,000 Haemonchus contortus larvae. Prostaglandin was infused intravenously 25, 50 and 75 days after infection for four hours at a rate of 5 micrograms/kg/minute and the egg counts in the faeces were determined daily for 110 days. Treatment on days 50 and 75 was followed by a significant rise in egg count lasting 19 and 12 days respectively. This observed rise seems to be related to a resumption of development of arrested larvae induced by prostaglandin treatment, and a hypothesis is proposed to explain its initiation.

Effects of intracerebroventricular administration of neurotensin, substance P and calcitonin on gastrointestinal motility in normal and vagotomized rats.

The effects of intracerebroventricular (ICV) vs. intravenous (IV) injection of neurotensin, substance P and calcitonin on intestinal myoelectrical activity were examined in fed rats. ICV administered neurotensin and calcitonin restored the 'fasted' pattern of intestinal activity, i.e. the migrating myoelectric complex (MMC) at a dose as low as 12 and 0.2 pmol, respectively, whereas substance P only reduced significantly (P less than 0.01) the duration of the postprandial pattern when injected ICV (48 pmol). Administered systemically at doses 100 times higher than the smallest active doses by the ICV route, calcitonin induced a fasted pattern, while neurotensin and substance P did not modify the fed pattern. The effects of ICV administration of neurotensin and calcitonin were abolished after vagotomy but the shortening effect of substance P on the duration of the postprandial pattern was still present. It is concluded that these three neuropeptides act centrally to control the pattern of intestinal motility in fed rats by shortening the 'fed' pattern for substance P and by restoring the MMC pattern for calcitonin and neurotensin, this last effect being mediated by the vagus.