PubMed Health⌕ Search

Biomedical subjects

C Rozé

Publications and source records attributed to C Rozé.

At least 91 records · Page 5Linked to original sources
PubMed1987

Comparative effects of pirenzepine and atropine on pancreatic secretion in conscious rats.

The effects of pirenzepine and atropine on basal pancreatic exocrine secretion were studied in conscious rats fitted with a chronic pancreatic fistula. Pirenzepine was about 50 times less potent than atropine on a molar basis in inhibiting pancreatic secretion (respectively 44x for volume and 51x for protein output), while the efficacies of both drugs were in the same range. These results indicate that basal pancreatic secretion in vivo is mainly regulated by muscarinic mechanisms poorly sensitive to pirenzepine, and analogous to the M2 receptors described by others in vitro.

Animals↗
PubMed1986

Etorphine inhibition of pancreatic exocrine secretion in rats: comparison with methadone.

The effects of etorphine, a potent opiate agonist without preferential affinity for mu, delta or kappa receptors, on exocrine pancreatic secretion were studied in rats fitted with chronic or acute pancreatic fistulas and compared to those of methadone, a well-documented mu agonist. In conscious rats etorphine (3 micrograms/kg s.c.) inhibited basal pancreatic secretion by about 50% for volume and bicarbonate output and by 70% for protein output. Pancreatic secretion returned to its basal level within 2 h. Methadone (5 mg/kg s.c.) was about equipotent but the inhibition lasted longer. The effects of both etorphine and methadone were completely antagonized by naloxone (1 mg/kg s.c.) and to a lesser extent by diprenorphine (10 microgram/kg s.c.). Yohimbine did not suppress the inhibitory effect of etorphine on protein output but showed some antagonism against the effects of etorphine on water and bicarbonate output. In anaesthetized rats etorphine (3 micrograms/kg) inhibited the pancreatic secretion stimulated by 2-deoxy glucose, a centrally acting vagal stimulatory agent, by 50-60% for volume and bicarbonate output and totally for protein output. The same dose of etorphine did not inhibit the pancreatic secretion evoked by vagal electrical stimulation, a peripheral stimulus. Methadone (5 mg/kg) inhibited the pancreatic secretion stimulated by 2-deoxy glucose to the same extent, but for a longer time than etorphine, and at the same dose did not suppress the pancreatic pancreatic response to vagal electrical stimulation. The inhibitory effects of etorphine and methadone in anaesthetized rats were completely suppressed by naloxone (1 mg/kg s.c.) and only reduced by diprenorphine (10 micrograms/kg s.c.).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1985

[Central inhibition of external pancreatic secretion by D-ala-2-metenkephalinamide in rats].

Intracerebroventricular injections of D-Ala-2-Metenkephalinamide (D Alamide), a slowly metabolized Metenkephalin analogue, were made to conscious rats equipped with a chronic pancreatic fistula allowing the collection of pure pancreatic juice in its entirety. D Alamide induced a dose-related decrease in the volume of basal pancreatic secretion, as well as of bicarbonate and protein outputs. The effective doses of D Alamide were of the same order of magnitude as those necessary to induce analgesia or to decrease intestinal transit time in rats, as reported by others. The effect of D Alamide was totally blocked by naloxone, an opiate antagonist known to easily traverse the blood-brain barrier, while no blockade was found with naloxone methyl-bromide, an opiate antagonist which traverses the blood-brain barrier poorly and thus acts only peripherally. These results strongly suggest that the inhibition of pancreatic secretion induced by D Alamide is a central effect.

Analgesics↗
PubMed1985

The effect of ranitidine on exocrine pancreatic secretion in the rat.

The effect of the H2-receptor antagonist ranitidine on pancreatic exocrine secretion was studied in the rat. In anaesthetized animals with acute fistulas pancreatic secretion was induced by central (2-deoxy-D-glucose, 2-DG) or peripheral (acetylcholine) cholinergic stimulants and by cholecystokinin and secretin. In some experiments cimetidine was used as a reference compound. Ranitidine (20 mg X kg-1 intraperitoneally) did not change neither basal secretion nor the response to the combined hormonal stimulation. On the contrary, it significantly increased 2-DG and acetylcholine-stimulated secretion, whereas cimetidine (100 mg X kg-1 intraperitoneally) inhibited the pancreatic response to 2-DG. The different behaviour of the two H2-antagonists suggests that the effect of ranitidine is independent of the H2-receptor blockade and most probably connected with the cholinergic-like action of the drug.

Acetylcholine↗
PubMed1984

[Effect of 5-thioglucose on external pancreatic secretion in rats. Comparison with 2-deoxyglucose].

The aim of this study was to compare the stimulation of the external pancreatic secretion induced in rats by two glucose analogs: 5-thio-glucose (5-TG) and 2-deoxy-glucose (2-DG). In rats with an acute pancreatic fistula, 5-TG and 2-DG induced a dose-related increase in outputs of sodium (reflecting the volume), bicarbonate and total protein of the pancreatic juice. The efficacy of both drugs was not significantly different. Maximal responses were obtained with 75 mg/kg 5-TG and 225 mg/kg 2-DG and were approximately 3.5 x (sodium), 5 x (bicarbonate) and 8.5 x (protein) the basal level. Dose-response curves to 5-TG were shifted to the left with respect to 2-DG. The DE50 was approximately 25 mg/kg for 5-TG and 60 mg/kg for 2-DG. The molar potency ratio was 2.5 x, 3.1 x and 3.3 x in favor of 5-TG, for sodium, bicarbonate and protein respectively. The potency, but not the efficacy, of 5-TG is thus greater than that of 2-DG in stimulating external pancreatic secretion.

Animals↗
PubMed1983

Modulation of stimulated pancreatic secretion by sympathomimetic amines in the rat.

Pancreatic secretion in anesthetized rats with acute fistulas was provoked by caerulein, acetylcholine, electrical stimulation of the vagus nerves or by 2-deoxy-D-glucose (2-DG). Venous infusions of norepinephrine, isoprenaline or dopamine inhibited the 2-DG-stimulated enzyme secretion but not that provoked by caerulein, acetylcholine or vagal electrical stimulation. Intracerebroventricular administration of norepinephrine or isoprenaline also inhibited 2-DG-stimulated enzyme secretion. It was confirmed that the amines stimulated water and electrolyte secretion by the pancreas in the order of potency isoprenaline greater than norepinephrine greater than dopamine. The results are consistent with a model whereby norepinephrine and isoprenaline exert their effect on pancreatic secretion via a central inhibition of vagal drive to the pancreas, together with a direct stimulating effect on water and electrolyte secretion at the level of pancreatic cells.

Acetylcholine↗
PubMed1983

Drug CRL 40 028-induced inhibition of pancreatic secretion in rats.

The drug CRL 40 028 increases spontaneous motility through an action on central adrenergic receptors. The effects of this drug have been tested in rats on the external pancreatic secretion induced by secretin, CCK, acetylcholine, vagal electrical stimulation or 2 deoxy-D-glucose. CRL 40 028 had no effect on basal secretion nor on secretion stimulated by agents acting directly on pancreatic secretory cells (secretin, CCK, acetylcholine), but decreased significantly secretion induced by central or peripheral stimulation of the vagus nerves. CRL 40 028-induced inhibition of 2 DG effect was reduced by yohimbine, suggesting a participation of alpha 2-adrenergic receptors in the action of CRL 40 028 on the exocrine pancreas secretion of rats.

Adrenergic alpha-Agonists↗
PubMed1982

Further support for the central origin of the gastric antisecretory properties of clonidine in conscious rats.

The effects of clonidine (CL) on interdigestive gastric acid secretion were studied in chronic gastric fistula rats and compared with those of St 91, a CL-like drug which does not cross the blood-brain barrier. CL induced a dose-dependent inhibition of gastric acid output when administered s.c. (ED50 13.5 micrograms X kg-1), in the lateral ventricle of the brain (ED50 5.80 micrograms X kg-1) or in the cisterna magna (ED50 0.49 micrograms X kg-1). St 91 and several alpha-adrenergic antagonists administered subcutaneously also inhibited gastric acid secretion dose dependently. Decreasing activities were prazosin greater than St 91 greater than phentolamine greater than yohimbine greater than piperoxan; phenoxybenzamine was a poor inhibitor. The anti-secretory properties of CL on basal secretion were antagonized by yohimbine and piperoxan. Other drugs either did not antagonize (phentolamine) or potentiated (phenoxybenzamine, prazosin) the CL effect, while yohimbine and phenoxybenzamine potentiated the response to St. 91. CL had no activity on methacholine while it drastically inhibited 2-DG-, histamine- and pentagastrin-stimulated gastric secretion. The inhibitory activity of CL on histamine stimulation was significantly decreased by yohimbine but not by phentolamine. These results confirm that the CL inhibition of the gastric acid secretion in unanesthetized rats is mediated at least partly through the stimulation of alpha 2-adrenergic receptors. Most of the data favour a major role of the CNS in the antisecretory activity of CL and suggest the possibility that most of the receptors involved are located in the medulla oblongata.

Adrenergic alpha-Antagonists↗
PubMed1982

Methadone inhibition of vagally induced pancreatic and gastric secretions in rats: central and peripheral sites of action.

Pancreatic and gastric secretions after stimulation with acetylcholine, electrical vagal stimulation or 2-deoxyglucose injection were studied in anesthetized rats. The effects of methadone on these secretions were investigated. Maximal stimulation of pancreatic secretion by acetylcholine was not affected by methadone. Gastric acid stimulation by acetylcholine was only slightly decreased by methadone (30% or less). Electrical vagal stimulation of pancreatic and gastric secretions was progressively and dose-dependently decreased to a maximum of 50% by methadone. Maximal stimulation of pancreatic and gastric secretions by 2-deoxyglucose was completely suppressed by methadone with an ID50 of about 1 mg/kg and an ID100 of about 2.5 mg/kg for both secretions. It is concluded that methadone inhibits vagal stimulation of digestive secretions by acting both centrally and peripherally (probably by inhibiting the release of acetylcholine from vagal fibers). The central mechanism appears to be more important, since it occurs with lower doses and can produce complete suppression of secretion.

Acetylcholine↗
PubMed1982

Ultrastructural study of pancreatic B cell regeneration in newborn rats after destruction by streptozotocin.

An ultrastructural study of endocrine cells was performed in the pancreas of rats treated with a single dose of streptozotocin on the day of birth. Most of the B cells present at birth were destroyed by streptozotocin but some survived and could again synthesize insulin after eliminating their altered fragments in phago-lysosome structures. New B cells were produced primarily by the formation of new islets from the small pancreatic ducts. A study of mitosis in colchicine treated animals showed that most B cells present on day 4 were formed by mitosis of undifferentiated cells. No significant division of preexisting differentiated B cells could be shown in streptozotocin treated rats. B cell regeneration in this newborn rat model is thus explained primarily by budding of new islets from the ducts.

Animals↗
PubMed1982

Inhibition of gastric and pancreatic secretions by cerebroventricular injections of gastrin-releasing peptide and bombesin in rats.

It has been suggested that mammalian gastrin-releasing peptide (GRP) and bombesin (BBS) might inhibit gastric secretion by a central nervous system action. The present investigations were intended to define the gastric effect and to look for an effect on the exocrine pancreas. Wistar male rats were provided with a chronic cannula allowing cerebroventricular injections in the 3rd ventricle, and with chronic gastric and/or pancreatic fistulas allowing the collection of gastric and/or pancreatic secretions in conscious animals. Both basal secretions were studied. Gastric secretion was stimulated with a 75 mg/kg s.c. injection of 2-deoxyglucose (2-dGlc). The dose range of bombesin was 0.01-1 microgram (6-600 pmol) and GRP was 0.01-10 microgram/rat (3.5 pmol to 3.5 nmol). A significant dose related decrease of basal gastric secretion was observed with the two peptides. The gastric acid response to 2-dGlc was inhibited by both peptides in a dose-related fashion and the reduction of gastric acid output mainly resulted from a decrease in the volume of gastric juice. The exocrine pancreatic secretion was also decreased by 30-55% after GRP but the BBS inhibitory effect was poorly dose-related. No significant difference was found after removal of gastric secretion, indicating that most of the pancreatic inhibition was independent of gastric secretion.

Animals↗