PubMed Health⌕ Search

Biomedical subjects

C Rozé

Publications and source records attributed to C Rozé.

At least 55 records · Page 3Linked to original sources
PubMed1994

[Cephalic phase of gastric secretion in dogs. Effect of palatability and caloric intake].

The purpose of this study was to analyze the relative part of the cephalic phase in the gastric secretory and circulating gastrin responses to meals of variable composition and palatability in dogs. Meal palatability was quantified by measuring the ingestion rate of a fixed amount of food. By progressively increasing the amount of carbohydrates or lipids added to a normal meat meal, it was possible to obtain eleven meals of progressively decreasing ingestion rate. When were offered as sham-feeding these eleven meals in dogs fitted with a cervical esophagostomy and a gastric fistula, gastric acid response decreased only after meals of very small ingestion rates. Moreover, neither gastrin, nor gastric pepsin responses changed significantly with ingestion rate of the sham-fed meals. By subtracting the response to sham-fed meals from the response to real meals of identical composition, it was possible to calculate the non-cephalic part of gastric responses. The non-cephalic part of gastric acid secretion and of circulating gastrin was significantly correlated to calorie intake; the slope of the best fitting regression line was greater after lipid meals than after carbohydrate meals. The non-cephalic part of pepsin secretion was very small, if any, and its level was not correlated to the amount of ingested calories. This work suggests that palatability has very little influence on gastric secretion control in dogs.

Animals↗
PubMed1993

Simultaneous assessment of liquid emptying and proximal gastric tone in humans.

BACKGROUND: Barostat is the only technique that allows assessment of gastric tone in humans. Our aim was to simultaneously assess gastric emptying and relaxation in response to a liquid meal. METHODS: Gastric tone was monitored using an electronic barostat in six healthy subjects after three liquid meals (200 mL, 400 mL, 600 mL, 1 kcal/mL). Scintigraphic imaging was obtained by using double isotopic labeling (technetium 99m for liquid of the 200 mL meal and xenon 133 for air into the barostat). RESULTS: Profound gastric relaxation was detected in every subject. The duration of proximal gastric relaxation increased with meal size. The proximal stomach remained relaxed through the duration of gastric emptying. Gastric tone returned to the fasting values simultaneously with completion of liquid emptying. Repeated measures after the 200-mL meal showed that amplitude (i.e., maximal volume change) and duration of relaxations were reproducible. However, the presence of the bag slightly accelerated gastric emptying and modified the intragastric distribution of the meal. CONCLUSIONS: The barostat is a sensitive and reproducible technique to measure gastric relaxation following liquid meals in humans. The results also suggest that the role of gastric tone as the driving force of gastric emptying of liquids has been overestimated.

Adult↗
PubMed1993

Mechanism of neurotensin stimulation of external pancreatic secretion in the rat.

The gut and brain peptide neurotensin has been claimed to directly or indirectly stimulate external pancreatic secretion. The purpose of this study was to analyze the mechanism of the neurotensin effect on external pancreatic secretion in the rat. The pancreatic dose-response curve to 40-min venous infusions of neurotensin 1-13 (0.1-10 micrograms/kg-h = 0.06-6 nmol/kg-h) was biphasic; the maximal response occurred at 3.16 micrograms/kg-h and reached approximately 30% of the maximal response to cholecystokinin (CCK). The ED50 was 0.27 micrograms/kg-h (= 0.16 nmol/kg-h) for bicarbonate and 0.45 micrograms/kg-h (= 0.27 nmol/kg-h) for protein output. Pancreatic secretion in response to each neurotensin dose increased steadily during the infusion and peaked 20-40 min after the end of infusion. Atropine and hexamethonium suppressed the stimulatory effect of neurotensin on volume, bicarbonate, and total protein output (p < 0.01). The CCKA receptor antagonist L364718 decreased by 80% sodium and bicarbonate response (p < 0.01) and suppressed protein response (p < 0.01) to neurotensin. Methadone reduced the response to neurotensin by 85%, vagotomy by 80%, and capsaicin pretreatment by 70%. The blockade of alpha 1-, alpha 2-, and beta-adrenoreceptors or of CCKB receptors did not change the neurotensin effect. We conclude that the mechanism of neurotensin stimulation is indirect and neurally mediated and involves nicotinic and muscarinic synapses, CCKA receptors, and, in part, capsaicin-sensitive sensory fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

[Sensory fibers sensitive to capsaicin can modulate secretion of the duodenal mucus. A morphometric study in rats].

Many in vitro and in vivo models have been used to study the modulation of intestinal mucosecretion. In such studies, quantification of mucus secretion is usually difficult, due to several technical problems. Whether sensory mechanisms participate in the modulation of intestinal mucosecretion remains unknown. The development and assessment of a morphometric method with computer assisted image analysis that allows to detect and quantitate mucin secretion by duodenal goblet cells are reported. Using this method, the secretory effect of pilocarpine on villus and crypt goblet cells was confirmed. We also determined whether sensory neurons can regulate intestinal mucosecretion by using capsaicin, a vegetal neurotoxin specific of a subpopulation of afferent primary sensory neurons. Intravenous capsaicin administration (10 micrograms/kg) increased mucus secretion by the goblet cells of the duodenal crypts. This suggests that sensory neurons may modulate duodenal mucin secretion. The "local effector function" of these neurons might be involved, in part through the release of substance P because exogenous substance P was able to increase mucin excretion by goblets cells of duodenal villi. Substance P, however, did not exactly mimic the capsaicin effects, suggesting that other factors were involved.

Animals↗
PubMed1993

[Effect of nalbuphine on external pancreatic secretion in rats].

Pancreatic secretion is controlled by neural and endocrine mechanisms. The administration of 2-desoxyglucose (2DG) to rats stimulates pancreatic secretion through a mainly vagal pathway, and provides an useful pharmacological model to study the agents (especially opiates and adrenergic drugs) which can modulate this neural pathway. In the present study, basal and 2DG-stimulated pancreatic secretion were measured in anesthetized rats. Nalbuphine had no effect on basal secretion; it antagonized 2DG-induced pancreatic stimulation in a dose-related fashion between 0.5 and 15 mg/kg iv. The effect of nalbuphine was suppressed by naloxone, but not by alpha and beta-adrenoceptor blocking agents, indicating an essentially opiate effect. In order to test whether an inhibition of kappa receptors participates in the nalbuphine effect, centrally or peripherally acting kappa agonists were associated with nalbuphine. Neither U50488H, nor ICI204448 changed 2DG stimulation and nalbuphine effect. In conclusion, the effect of nalbuphine on 2DG-stimulated pancreatic secretion was similar to that of methadone and buprenorphine, required larger doses, and seemed to mainly involve mu receptors.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1993

[Use of an electronic barostat for measurement of motor response of the proximal stomach to feeding and different nervous stimuli in man].

Electronic barostat allows to measure volume variations of an intragastric air-filled bag maintained at a low constant pressure level, reflecting gastric tone variations. The aims of the present study were to record physiologic variations of gastric tone in humans a) in the fasting state, with and without different stimuli, and b) in the fed state. The bag was placed into the proximal stomach of healthy subjects and connected to the barostat. Volume variations were recorded in the basal state and in response to a) a balanced liquid meal (200 mL, 200 kcal, n = 8), b) sham feeding and sham feeding after cholinergic blockade (atropine 10 micrograms.kg-1 IV, n = 8), and c) graded antroduodenal distensions performed with a tandem balloon (n = 6). During fasting, the proximal stomach presented both a tonic and an intermittent phasic motor pattern (volume waves of 1.2 min maximal period). Meal ingestion was rapidly followed by a dramatic fall in proximal gastric tone (> 200% of preprandial volume within 11 +/- 5 min). After a meal, the intragastric bag returned to preprandial volume after 92 +/- 12 min (ranges: 75-110). Proximal gastric tone was not significantly modified by atropine or by sham feeding alone or after atropine. Antroduodenal distensions reproducibly induced volume dependent relaxations (r = 0.98, P < 0.001) with inhibition of the phasic activity. These results confirm the value of electronic barostat for the measurement of proximal gastric tone, and show that postprandial relaxation is not masked by a low volume liquid meal. Sham feeding does not appear to be an adequate stimulus to induce gastric relaxation. This suggests that vagal fibers involved in gastric relaxation are not the same (or have a higher stimulation threshold) than fibers involved in cephalic phase of gastric secretion.

Adult↗
PubMed1992

CRL41405: a drug with a new pharmacological profile on pancreatic exocrine secretion in the rat.

The recently described compound CRL41405 displays central effects suggesting possible antidepressive and awakening properties. In order to further analyze the pharmacology of this compound, its effects were studied on basal and stimulated pancreatic secretion in anaesthetized rats. CRL41405 alone (7-20 mg/kg, sc) had no effect on basal pancreatic secretion. Larger doses (67-200 mg/kg) increased basal secretion through the stimulation of cholinergic muscarinic receptors, the effect being antagonized by atropine. CRL41405 (20 mg/kg) suppressed the 2-deoxyglucose-induced (but not the acetylcholine-induced) stimulation of pancreatic secretion through an alpha-2 adrenoceptor inhibitory mechanism that was blocked by idazoxan (0.3 mg/kg, sc). In addition, a beta adrenoceptor mediated stimulation of sodium and bicarbonate excretion (blocked by propranolol) was evidenced when the alpha-2 inhibition was suppressed by idazoxan. Under alpha-2 adrenoceptor blockade, water and electrolyte stimulation by CRL41405 could be demonstrated on basal, 2-deoxyglucose-induced and acetylcholine-induced pancreatic secretion. This original profile makes CRL41405 a unique drug in pancreatic pharmacology.

Acetylcholine↗
PubMed1992

Effect of alpha 2-adrenoceptor agonists on gastric pepsin and acid secretion in the rat.

1. The purpose of the present study was to analyze the effects of the alpha 2-adrenoceptor agonists clonidine, guanabenz, detomidine and medetomidine on pepsin secretion in conscious rats provided with gastric chronic fistula and to compare this with acid secretion. 2. Basal interdigestive gastric secretion, which is mainly neurally driven in the rat, and the secretion directly stimulated by the two main stimulants of chief cells, cholecystokinin octapeptide (CCK8) and methacholine, were studied. 3. Basal secretion of pepsin and acid was inhibited by all four drugs with comparable EC50S. 4. CCK-stimulated pepsin and acid secretion was less sensitive than basal pepsin and acid secretion to alpha 2-adrenoceptor inhibition. 5. Methacholine-stimulated pepsin and acid secretion was not changed by clonidine and guanabenz; methacholine-stimulated acid was even marginally increased by clonidine. 6. These results do not favour the presence of alpha 2-receptors on chief cells in the rat stomach. They rather suggest that pepsin inhibition by alpha 2-adrenoceptor agonists is indirect and due to central or peripheral inhibition of the discharge of nerve fibres activating pepsin secretion.

Adrenergic alpha-Agonists↗
PubMed1991

Effect of modafinil on pancreatic exocrine secretion in the rat. A comparison with methadone.

Modafinil is a recently developed drug which increases wakefulness in several animal species and in man, an effect involving, at least in part, central adrenoceptors. In the present experiments, the effect of modafinil was studied on a model of neurally stimulated secretion, pancreatic secretion induced by 2-deoxyglucose (2DG) in the rat, and compared with that of the mu-opiate methadone. Modafinil induced a dose-related inhibition of 2DG-stimulated pancreatic secretion, reaching more than 80% after 250 mg/kg i.p. The modafinil effect was suppressed by idazoxan or by large doses of prazosin but not by naloxone. In addition modafinil (250 mg/kg i.p.) did not change the pancreatic response to electrical vagal stimulation. Methadone also potently suppressed 2DG-stimulated pancreatic secretion, but in contrast to modafinil, the methadone effect was blocked by naloxone, but not by the adrenoceptor antagonists idazoxan, prazosin and propranolol. It is concluded that modafinil decreases centrally 2DG-stimulated pancreatic secretion through a pathway involving alpha 1- and alpha 2-adrenoceptors, without an interaction with opiate receptors.

Adrenergic alpha-Antagonists↗
PubMed1991

Central and peripheral effects of prostaglandin E2 and enprostil on gastric acid secretion in the rat.

The intracerebroventricular (i.c.v.) administration of prostaglandin E2 (PGE2) inhibits gastric secretion at doses that are inactive by i.v. administration in the rat. The present study was undertaken to examine the central and peripheral effects of enprostil, a potent synthetic PGE2 analogue, on gastric acid secretion as compared to those of PGE2. We used conscious rats equipped with a chronic gastric fistula and a cannula to allow injection into the third ventricle of the brain. Gastric acid output was measured under basal interdigestive conditions and during stimulation with submaximal doses of pentagastrin and histamine. Total inhibition of basal and stimulated gastric acid output was obtained after i.c.v. PGE2 and after i.c.v. or i.v. enprostil administration. After i.v. PGE2, the maximal observed inhibition was not greater than 50%. The ratio of ED50 values for i.v. administered to i.c.v. administered PGE2 was 64 or more, whereas the ratio of ED50 values for i.v. enprostil to i.c.v. enprostil was 9 to 13. Under all conditions studied, enprostil was more potent than PGE2 and this greater potency was more prominent after i.v. administration (ratio 250 to 2500) than after i.c.v. administration (ratio 10 to 400). The blockade of alpha 2-adrenoceptors by idazoxan did not suppress the inhibition of gastric secretion produced by i.c.v. PGE2 or enprostil. It is concluded that low doses of PGE2 inhibit gastric acid output mainly through a central mechanism, whereas low doses of enprostil potently inhibit gastric acid output through both a central and a peripheral mechanism. alpha 2-Adrenoceptors are not essential for the effect of i.c.v. prostanoids on gastric acid secretion.

Adrenergic alpha-Antagonists↗
PubMed1991

Antisecretory and anti-ulcer effects of morphine in rats after gastric mucosal aggression.

The effects of morphine on gastric secretion, barrier mucus and mucosal lesions were studied in pylorus-ligated rats treated with the ulcerogenic agents, indomethacin, aspirin or taurocholic acid. All three ulcerogenic agents induced significant mucosal lesions. Morphine decreased gastric acid secretion and suppressed the aspirin- and taurocholic acid-induced, but not the indomethacin-induced mucosal lesions. These results suggest that the ulcerogenic mechanisms of indomethacin and the other agents are not identical. Moreover the antiulcer effect of morphine appears to be mediated by an increased barrier mucus level: the amount of Alcian blue bound to the mucosa, an indirect estimate of the adherent mucus layer, was increased by morphine and correlated with its protective effect. All morphine effects were reversed by naloxone.

Animals↗
PubMed1991

Synthetic CCK8 analogs with antagonist activity on pancreatic receptors: in vivo study in the rat, compared to non-peptidic antagonists.

The cholecystokinin octapeptide (CCK8)-derived synthetic peptides Boc-Tyr(SO3H)-Nle-Gly-DTrp-Nle-Asp-O-CH2-CH2-C6H5 (JMV179) and Boc-Tyr(SO3H)-Nle-Gly-DTrp-Nle-Asp-NH-CH2-CH2-C6H5 (JMV167) are antagonists of peripheral cholecystokinin (CCK) receptors in vitro. In the present study, antagonist activity of these peptides was studied on rat pancreatic secretion in vivo, and compared to those of other peptidic molecules and to the non-peptidic antagonists L364718, D-, L-, DL-lorglumide, and proglumide. The decreasing order of antagonist potencies on amylase release in vitro was L364718 greater than JMV179 greater than lorglumide greater than JMV167 greater than proglumide; JMV179 was 25 times less potent than L364718 and 300 times more potent than JMV167. The decreasing order of antagonist potencies on protein output in pancreatic juice in vivo was L364718 greater than JMV167 greater than JMV179 greater than lorglumide greater than proglumide; JMV167 was two times more potent than JMV179 and only 8 times less potent than L364718. Increased potency of JMV167, relative to JMV179 under in vivo conditions, is probably due to the slower rate of catabolism of the phenylethylamide group, relative to the phenylethylester group, since the metabolite issued from hydrolysis of the ester bond was totally inactive. This study shows that it is possible to obtain peptidic CCK antagonists, which are active and potent in vivo, and provides a quantitative measurement of potency changes occurring in vivo for several peptidic and non-peptidic antagonists.

Amino Acid Sequence↗
PubMed1991

[Action of neurotensin on duodenal alkaline secretion in rats. Comparison with pancreatic and gastric secretion].

Neurotensin is released from endocrine N cells of the ileum after meals, and might take part in the regulation of bicarbonate secretion by the pancreas and duodenum. The aim of this study was to define the effect of neurotensin on duodenal bicarbonate secretion, in comparison with its effect on gastric and pancreatic secretions. Neurotensin produced a dose-related increase of duodenal bicarbonate secretion with an ED50 of 60 pmol/kg.h. The maximal effect (about 2 times the basal level) was observed with 600 pmol/kg.h. Equimolar doses (600 pmol/kg.h) of xenopsin, neuromedin N, neurotensin 8-13 produced the same effect as neurotensin 1-13. Neurotensin fragments 1-11 and 9-13 (600 pmol/kg.h) had no significant effect on duodenal bicarbonate secretion. Indomethacin, atropine, naloxone, or the CCK antagonist L364,718 had no effect on neurotensin-stimulated bicarbonate secretion. Hexamethonium and vagotomy reduced the neurotensin effect by about 50 percent (P less than 0.05). Neurotensin produced a dose-related increase of pancreatic bicarbonate secretion with an ED50 of 150 pmol/kg.h, a decrease of gastric acid secretion with an ED50 of 2,400 pmol/kg.h, and a decrease of gastric pepsin secretion with an ED50 of 2,760 pmol/kg.h. This study shows that neurotensin stimulates duodenal bicarbonate secretion in doses which may be physiological. This biological activity depends on the presence of the C-terminal 8-13 fragment. The mechanism is complex, and depends, for approximately half, on vagal fibers (sensitive or motor), nicotinic synapses, and a non cholinergic effector. The other half of the effect, still unexplained, could be a direct effect on mucosal cells. Pancreatic and duodenal bicarbonate secretions were more sensitive to neurotensin than gastric secretion (acid and pepsin).

Animals↗
PubMed1990

Effects of buflomedil and its two derivatives, CRL40634 and CRL40598, on pancreatic exocrine secretion in the rat.

Buflomedil is a vasoactive drug used in the treatment of peripheral vascular disease, and seems to be an antagonist of both alpha 1- and alpha 2-vascular adrenoceptors. CRL40634 and CRL40598 are metabolites of buflomedil and also possess vasoactive properties. The purpose of this study was to investigate whether buflomedil, CRL40634 and CRL40598 have antagonist activity on the alpha 2-adrenoceptors involved in the inhibition of exocrine pancreatic secretion. In acute pancreatic fistula rats, buflomedil, CRL40634 and CRL40598 did not suppress the inhibitory effect of clonidine against 2-deoxy-glucose-induced pancreatic secretion. However, all three drugs inhibited 2-deoxy-glucose-induced pancreatic secretion, their order of potency being CRL40598 greater than CRL40634 greater than buflomedil.

Acetylcholine↗