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Biomedical subjects

C Rozé

Publications and source records attributed to C Rozé.

At least 109 records · Page 6Linked to original sources
PubMed1981

Clonidine inhibition of pancreatic secretion in rats: a possible central site of action.

The effects of clonidine on pancreatic secretion were studied in rats fitted with chronic or acute fistulas. Subcutaneous and intracerebroventricular injections of clonidine in conscious rats induced a dose-dependent inhibition of basal pancreatic secretion involving volume, bicarbonate output and protein output with an ED50 of about 10 micrograms/kg. Clonidine inhibition of pancreatic secretion was not dependent on the associated inhibition of gastric acid output. In conscious rats, the pancreatic inhibitory effect of clonidine was completely antagonized by yohimbine and slightly by piperoxane and prazosin. Propranolol, mianserin, naloxone and cimetidine did not antagonize the clonidine effect. Clonidine decreased the basal pancreatic secretion in anaesthetized rats and this action was completely reversed by yohimbine. Clonidine inhibited the pancreatic secretion stimulated by 2-deoxyglucose. This effect was reversed by yohimbine, while prazosin had no effect. Clonidine did not inhibit the pancreatic secretion induced by electrical stimulation of the vagus nerves. These results suggest that clonidine inhibition of pancreatic secretion is mediated through alpha 2-adrenergic receptors, and at least in part by a central nervous system mechanism. Yohimbine alone increased basal pancreatic secretion in conscious rats. This suggests that alpha 2-adrenergic receptors might be involved in the physiological nerve tone to the pancreas.

Animals↗
PubMed1981

Histogenesis of the endocrine pancreas in newborn rats after destruction by streptozotocin. An immunocytochemical study.

Endocrine pancreatic tissue in newborn rats was studied 1 to 17 days after the destruction of B cells by an injection of streptozotocin. Regeneration of insulin cells was observed four days after streptozotocin injection, which was followed by recovery from the diabetic state and an increased pancreatic insulin content. Regeneration was characterised by new islets budding from small ducts. The pancreas of newborn rats, like the embryonic pancreas, thus retains a capacity to form endocrine tissue, although some degree of reduplication of preexisting B cells may also be involved in the process. Newborn rats injected with streptozotocin constitute an interesting model for the study of factors which may act on the regenerative potential of pancreatic endocrine tissue in the diabetic state.

Animals↗
PubMed1980

Response of rat exocrine pancreas to chronic pulmonary ethanol intoxication.

Rats were intoxicated over a 32-day period by continuous exposure to an ethanol-enriched atmosphere. Under these conditions, body weights increased up to day 26 and blood ethanol levels increased to approximately 2 g/liter. Pancreatic and hepatic histologies were normal. Amylase levels and total pancreatic protein decreased, while lipase levels rose. These changes appear to be independent of the caloric balance of the diet.

Alcoholic Intoxication↗
PubMed1980

Neurohumoral control of gastrointestinal motility.

The progress of gastrointestinal physiology is presently dominated by the concept of neuroendocrine regulation and the control of motility is in keeping with this concept. Progress in biochemistry, immunocytochemistry and radioimmunoassay in the past few years has produced a whole new collection of peptide molecules extracted from the digestive tract. Two facts are evident from these new data: (i) many peptides in the gastrointestinal tract are present in both endocrine cells and nerve fibers, and (ii) many peptides are found in both the brain and the gastrointestinal tract. There is thus a large wave of interest in the so-called brain-gut axis and in the relations between brain and gut and between nerves and hormones. The motile system of the gastrointestinal tract is a complex whole having several organizational levels. The morphological, fixed structure is a "cable" network comprising smooth muscle and intrinsic and extrinsic nerves. Control feedback loops may be evidenced at all levels-muscular, intrinsic, ganglionic and central. Local concentrations of circulating (endocrine) or paracrine peptides may act as modulators of this basic pattern by contributing to the depolarization or the hyperpolarization of smooth muscle cell membranes. The mode of action of these peptides reveals at least two different kinds of receptor sites: one on the smooth muscle cells and the other on the axons or cell bodies of intramural excitatory or inhibitory neurons. In addition, central nervous system effects may centrally modulate the long pathway reflexes travelling in the main vagosympathetic trunks. It is no longer possible to separate completely the neural from the hormonal in studying motility control. The whole neuroendocrine control complex must be investigated.

Animals↗
PubMed1980

Central inhibition of basal pancreatic and gastric secretions by beta-endorphin in rats.

The effects of intracerebroventricular injections of synthetic ovine beta-endorphin were tested in conscious rats with gastric and pancreatic fistulas. In the range of 0.8 to 25 microgram injected in the third ventricle of the brain, basal gastric and pancreatic secretions were strongly inhibited in a dose-dependent manner. Pancreatic volume, bicarbonate output, and total protein output were similarly inhibited, while the bicarbonate concentration was only slightly changed. Similar effects were noted after the administration of morphine. In the present model system, morphine was 20-30 times less active than beta-endorphin on a molar basis. Beta-Endorphin inhibition of pancreatic secretion was reversed by naloxone, suggesting that opiate receptors are involved in this phenomenon. Gastric acid secretion participated in the pancreatic effects of beta-endorphin to only a slight extent, since pancreatic inhibition by the endorphin was decreased only slightly in rats with gastic fistula in which gastric juice was diverted and did not reach the duodenum. The comparison of intravenous and intraventricular injections of beta-endorphin and morphine suggested that the observed inhibitions originated in the central nervous system. No effects were detected after the administration of alpha-endorphin, Met-enkephalin or Leu-enkephalin, although pancreatic secretion was measurably inhibited by long-acting synthetic enkephalin analogues.

Animals↗
PubMed1979

Occurence and cytodifferentiation of mucopolysaccharide secreting cells in the pancreas of children with nesidioblastosis.

Large numbers of mucopolysaccharide secreting cells were found in the pancreatic tissue of children with nesidioblastosis. Ultrastructural studies showed that mucus cells contained secretion granules and a characteristic smooth endoplasmic reticulum composed of an array of anastomosed tubules. The periodic acid - thiocarbohydrazide - silver reaction demonstrated the presence of glycogen in the hyaloplasm and of polysaccharides in secretion granules, the Golgi apparatus and in vesicles. A hypothesis is proposed, according to which mucus cells differentiate from a pancreatic stem cell common to both endocrine and exocrine tissues, through a mitochondria-rich intermediate cell stage.

Adenoma, Islet Cell↗
PubMed1979

Action of tiadenol and clofibrate on biliary excretions of cholesterol and bile salts in rats.

Biliary excretion of cholesterol, phospholipids and bile salts, and the excretion of labeled cholesterol injected intravenously were studied in rats treated for 1 or 3 weeks with the hypolipidemic drugs tiadenol and clofibrate. Total biliary cholesterol concentration and output decreased in treated rats, and the cholesterol solubility ratio increased. The excretion of labeled bile salts increased with both drugs; the excretion of labeled cholesterol increased with clofibrate and tended to decrease with tiadenol. The ratio of labeled bile salts/labeled cholesterol was higher with tiadenol than with clofibrate.

Animals↗
PubMed1978

[Action of somatostatin and 3 analogs on external pancreatic secretion in the rat].

The effect os somatostatin (SS) and of its analogs D Trp 8-SS and Asn 5-SS was studied upon the external pancreatic secretion of the Rat after stimulation by 2 deoxy-D-glucose. The secretion of sodium and bicarbonate was similarly inhibited by all four peptides. The analog D Trp 8-SS was more effective in inhibiting pancreatic protein excretion.

Animals↗
PubMed1978

Parietal cell vagotomy in dogs. A comparative study of the effects on gastric secretion and antral muscle contraction.

The aim of this work was to further investigate whether it is possible, through parietal cell vagotomy (PCV), to obtain both a complete suppression of the gastric secretory response to vagal impulses and to retain a normal contractile response of the antral muscle. Acid and peptic secretions, the electrical activity and the force of circular antral contractions were simultaneously studied in dogs, before and after PCV, under 2-deoxy-D-glucose (2DG) and pentagastrin (PG) stimulation. After PCV, the response to 200 mg/kg 2DG was reduced by about 70% for acid and 80% for pepsin; the slopes of the dose-response curves were significantly reduced after PCV. The slope of the regression line pepsin/acid after 2DG was decreased following PCV. The mean acid response to PG was reduced about 50% after PCV. Plasma immunoreactive gastrin increased following 2DG, and the variations were identical before and after PCV. The gastric control electrical activity in basal conditions (fasted dogs) and following 2DG was similar before and after PCV. The antral contractile response to 2DG was reduced by about 40% after PCV. In conclusion, when PCV induced an 80% reduction in the gastric secretory response to maximal vagal stimulation by 2DG, the contractile antral response was not entirely normal. This effect might be due either to a partial antral denervation or to some intrinsic influence of the denervated gastric body upon the strength of antral contractions.

Animals↗
PubMed1978

Methadone blockade of 2-deoxyglucose-induced pancreatic secretion in the rat.

The effects of methadone on pancreatic exocrine secretions in the rat were tested under basal conditions and after hormonal stimulation by secretin and caerulein or after stimulation of the differentially acting cholinergic agents acetylcholine, 2-deoxyglucose, and electrical stimulation of the vagus. Methadone had no effect on basal hydroelectrolytic secretion. It decreased basal enzyme secretion very slightly under our experimental conditions. The stimulatory effects of 75 mg of 2-deoxyglucose per kg were completely blocked by methadone at 5 mg per kg and this blockade was reversed by nalorphine at 6 to 9 mg per kg. It was found that there are doses of methadone (100 microgram) which block 2-deoxyglucose effects when injected into brain ventricles but are ineffective when systemically introduced. The effects of secretin, caerulein, acetylcholine, and electrical stimulation of the vagus were not depressed by methadone. These results strongly suggest that the methadone blockade of 2-deoxyglucose effects occurs at a central level and is mediated by narcotic drug receptors.

Acetylcholine↗