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M J Fargeas

Publications and source records attributed to M J Fargeas.

46 records · Page 3Linked to original sources
PubMed1984

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.

Animals↗
PubMed1984

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.

Adrenergic alpha-Antagonists↗
PubMed1984

Time-related effects of benzodiazepines on intestinal motility in conscious dogs.

The effects of diazepam and GABA on intestinal motility were investigated in fasted dogs fitted with strain-gauge transducers. Injected intravenously at 9.00 and 16.00 h, diazepam (0.5 mg kg-1) affected intestinal motility only during darkness i.e. from 19.00 to 7.00 h. These jejunal motor effects which were mimicked by GABA, (0.3 mg kg-1 i.v.) corresponded to a disruption of the migrating myoelectric complex (MMC) with an increased contractile activity. These results demonstrate that benzodiazepines affect the intestinal motility in dog and suggest that the effects are related to sleep-stages.

Animals↗
PubMed1984

The involvement of opiate receptors in the effects of trimebutine on intestinal motility in the conscious dog.

The effects of intravenous (i.v.) vs intracerebroventricular (i.c.v.) administration of trimebutine on the motility of the small intestine and colon of fasted dogs were assessed using chronic electromyography. Trimebutine, injected intravenously, stimulated small intestinal motility, by inducing a propagated phase of regular spike activity, and inhibited colonic motility for some 4 h. These effects were not reproduced by i.c.v. administration which disrupted the cyclic motor profile of the small intestine for about 2.5 h and did not modify colonic motility. The stimulation of the small intestine motility induced by i.v. administration of the drug was blocked by previous i.v. but not by i.c.v. administration of naloxone. It was concluded that in the dog, the effects of trimebutine on the small intestine but not on the colon, involve peripheral opiate receptors.

Action Potentials↗
PubMed1984

Comparative effects of morphine and cyclazocine on gastrointestinal motility in conscious dogs.

The effects of intravenous (i.v.) and intracerebroventricular (i.c.v.) administration of two opiate-like drugs, morphine and cyclazocine on gastrointestinal motility were investigated in conscious fasted dogs chronically fitted with strain gauge transducers on the antrum, the jejunum and the colon. Intravenous administration of morphine (100 micrograms.kg-1) induced a disorganization of the cyclic motility of the antrum, a premature phase of regular activity on the jejunum and a stimulation of colonic motility. Intracerebroventricular administration of morphine at a 10 times lower dose induced a short (10-15 min) stimulation of gastric motility followed by a prolonged (2-3 hr) inhibition associated with a disorganization of the jejunal motility and a stimulation of colonic motility. Cyclazocine at the same doses (10 micrograms.kg-1) induced identical effects after administration by i.v. and i.c.v. routes which consisted of an inhibition of gastric and jejunal motility and a stimulation of colonic motility. These results show peculiar motor responses, at each level of the digestive tract, to central and peripheral administration of an opiate-like drug.

Animals↗
PubMedDate not supplied

Calcitonin gene-related peptide: brain and spinal action on intestinal motility.

The effects of intracerebroventricular (ICV) and intrathecal (IT) administration of calcitonin gene-related peptide (CGRP) on intestinal motility were examined in conscious rats chronically fitted with intraparietal electrodes in the duodeno-jejunum and a cannula in a cerebral lateral ventricle or catheter in the subarachnoid space. ICV administration of CGRP (0.5-10 micrograms) restores the fasted pattern of intestinal motility in fed rats in a dose-related manner. Intrathecal administration of CGRP or calcitonin also induces fasted pattern but after a 30 min delay. These effects persisted after transection of the spinal cord and no change in intestinal motility appeared after intravenous administration of CGRP at a dose effective when given IT. This study suggests that CGRP, as calcitonin, has a neuromodulatory role in the control of intestinal motility at both brain and spinal cord levels.

Animals↗
PubMedDate not supplied

Involvement of dopamine in the central effect of neurotensin on intestinal motility in rats.

The effects of intracerebroventricular (ICV) administration of neurotensin (NT) before a meal on intestinal postprandial motility were examined in conscious rats chronically fitted with intraparietal Nichrome electrodes in the duodeno-jejunum. The effects were compared with those of two analogues, [D-Tyr11]NT and [D-Trp11]NT, resistant to degradation by brain peptidases. NT (10 micrograms ICV) delayed the occurrence of postprandial disruption of duodenal motility and blocked it on the jejunum. [D-Tyr11]NT and [D-Trp11]NT (1 microgram ICV) elicited the same effects but at a ten-fold lower dose. NT administered peripherally just before a meal significantly lengthened the duration of the postprandial motor pattern. The central effect of NT on the fed pattern involved dopaminergic neurons as it was mimicked by dopamine, blocked by haloperidol and partly antagonized by either sulpiride or (+) SCH 23390. It is concluded that: 1) both D1 and D2 receptors are involved in the blocking effect of the postprandial disruption induced by central NT; 2) that [D-Tyr11]NT and [D-Trp11]NT are potent agonists at NT receptors in the brain.

Animals↗