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Biomedical subjects

R Laugier

Publications and source records attributed to R Laugier.

90 records · Page 5Linked to original sources
PubMed1980

Increased gastrin release in chronic calcifying pancreatitis and in chronic alcoholism.

Plasma gastrin levels were measured by radioimmunoassay before and after a test meal associated with 40 ml ethanol in 21 patients presenting with chronic calcifying pancreatitis, in 10 apparently normal subjects drinking since at least 5 years 100 g alcohol a day, in 14 subjects presenting hepatic alcoholic cirrhosis and in 18 apparently normal non alcoholic controls. Post-stimulation gastrin concentration were higher in chronic pancreatitis patients or in normal alcoholics (peak post-stimulation value: 74 +/- 41 and 74 +/- 43 pg/ml respectively) than in cirrhotics or non alcoholic controls (45 +/- 26 and 41 +/- 15 pg/ml respectively) (m +/- SD).

Adult↗
PubMed1980

Pancreatic acinar cells: electrophysiological evidence for stimulant-evoked increase in membrane calcium permeability in the mouse.

1. Membrane potential and resistance were measured in acini from superfused isolated segments of mouse pancreas using two micro-electrodes inserted into neighbouring acinar cells. Stimulation was carried out exposing segments to 5 x 10(-7) M-acetylcholine (ACh) or 3 x 10(-7) M-pentagastrin. 2. Sustained stimulation with ACh or pentagastrin caused sustained membrane depolarization and resistance reduction. For periods of stimulation up to 15 min there was no sign of desensitization. 3. Sustaind stimulation during exposure of the tissue to a Ca-free solution containing EGTA (ethylene glycol bis-(beta-aminoethyl ether)-N,N'-tetraacetic acid) resulted only in a transient depolarization and resistance reduction. 4. Removal of external Ca during sustained stimulation resulted in immediate hyperpolarization and increase in resistance. Readmission of Ca, still during exposure to ACh or pentagastrin, depolarized the membrane and reduced the resistance. Mn could not mimic this effect of Ca. 5. Removal of external Ca in the absence of stimulation evoked depolarization and membrane resistance reduction. 6. It is concluded that sustained stimulation of pancreatic acinar cells with cholinergic agents or peptides of the cholecystokinin-gastrin group evokes an increase in the Ca permeability of the plasma membrane. Ca entering the cells from the outside is important in maintaining ion channels in their open state, thus sustaining the stimulant-evoked depolarization and resistance reduction. The initial stimulant-evoked membrane response, however, seems to be triggered by release of Ca from internal stores and is independent of external Ca.

Acetylcholine↗
PubMed1979

Pancreatic response to secretion+CCK-PZ in European and North African adults and children.

Pancreatic response to intravenous secretin GIH (1CU/kg) +CCK-PZ (3CHRU/kg) was investigated in European and North African normal subjects. The pancreatic responses were compared in two groups of 38 normal male adults and in two groups of nine normal nurslings (less than 1 year). Body weight and age were similar in the two adult groups and in the two nursling groups. The peaks of volume, electrolytes, and enzymes were determined in samples of duodenal aspirate after hormonal stimulation. In adult subjects the flow rate and electrolytes were not statistically different in the two groups, while enzyme outputs were lower in the North African group -73% for lipase (P less than 0.001), -54% for phospholipase (P less than 0.01), and -35% for chymotrypsin (P less than 0.05). On the other hand, in both groups of nursling subjects all parameters of pancreatic secretion were identical. The difference in the pattern of the pancreatic response to exogenous hormonal stimulation observed between the two groups of adult subjects could be related to genetic or acquired differences. The second hypothesis is, however, the most probable because the pancreatic secretion was similar in both groups of nursling subjects.

Adult↗
PubMed1979

Inhibition of rat pancreatic secretion by neurotensin: mechanism of action.

The effect of neurotensin on rat pancreatic secretion was studied in the conscious animal as well as on pancreatic lobules. In vivo neurotensin induced a dose-related inhibition of both water and protein basal secretion. Protein secretion was much more depressed than fluid secretion. Neurotensin did not modify the pancreatic response to exogenous secretin or cholecystokinin-pancreozymin, or to intraduodenal infusion of HCl. On the other hand neurotensin totally inhibited the increase in volume as well as in protein output to an intraduodenal infusion of oleic acid, but did not change the delayed inhibitory effect on protein output. In vitro, neurotensin did not affect basal and cholecystokinin stimulated pancreatic secretion. These results indicate that: 1) neurotensin could interfere with the release of hormones from the gut (cholecystokinin, and possibly VIP), 2) neurotensin did not mimic the delayed protein inhibitory effect observed after administration of oleic acid.

Amylases↗
PubMed1977

Action of oleic acid on the exocrine pancreatic secretion of the conscious rat: evidence for an anti-cholecystokinin-pancreozymin factor.

The effects on exocrine pancreatic secretion of an intraduodenal infusion of oleic acid (2 ml in 60 min) has been assessed in conscious rats provided with a new type of duodenal cannula permitting the normal flow of pancreatic juice, but not of bile, between experiments.1. Intraduodenal oleic acid infusion induces an increased secretion of water and bicarbonate which is still significantly above basal values 90 min after the end of infusion. Protein output increased during the infusion, but protein concentration and output significantly decreased under basal levels 120 min and 150 min after infusion (respectively -63 and -57% of basal values at 150 min).2. No inhibition was found when oleic acid was introduced into the caecum or into the first 20 cm of ileum isolated from the rest of small intestine. On the contrary, inhibition of protein secretion was induced immediately by intra-ileal oleic acid infusion.3. Inhibition of protein secretion secondary to intra-ileal oleic acid infusion was transmitted from a donor rat to a receiver rat by means of a cross-circulation.4. It is concluded that oleic acid induces an immediate and long lasting increase in water and bicarbonate secretion. During the infusion of oleic acid, protein output is increased, followed by an inhibition. This delayed inhibition stems from the second part of the small intestine and was transferred from one rat to another by cross-circulation: it is speculated that oleic acid releases in the conscious rat (from the distal part of the small intestine) a hormonal factor inhibiting pancreatic secretion.

Animals↗
PubMed1976

Atropine-induced inhibition of the enhanced CCK release observed in alcoholic dogs.

As it has been previously shown, the pancreatic secretory response to an intraduodenal infusion of oleic acid is increased in animals accustomed to daily ethanol consumption compared to matched controls. This action has been verified in dogs provided with a Thomas cannula and consuming 2 g kg-1 ethanol or not, daily since 3 years. An intravenous infusion of 0.75 mg kg-1 h-1 of atropine suppresses the difference between alcoholic and non-alcoholic animals. Therefore, the increased release of CCK-PZ in response to meal, which is characteristic of chronic alcoholic animals, is under cholinergic control.

Alcoholism↗
PubMed1976

Canine exocrine pancreatic secretory changes induced by calcium or ethanol plus calcium intraduodenal infusion.

In dogs provided with chronic gastric and pancreatic fistulas (Thomas cannula), an 80-minute intraduodenal CaCl2 (0.6 mM/kg.) infusion against a background of secretin perfusion (GIH, 1.0 CU/kg./hr.) elicits a complex "pancreon" response consisting of both excitatory and inhibitory effects on the protein and alkaline components, respectively, of pancreatic secretion. It is postulated that these pancreatic secretion changes are the result of the interplay of released CCK and calcitonin. The lack of pancreatic secretion modifications when ethanol (0.7 mg./kg.) was added to the intraduodenal CaCl2 infusion suggests that the former counteracts the effects of the latter on the nerves and/or the endocrine cells of the gut. Ca++ concentration and output in pancreatic secretion did not change significantly either with the intraduodenal CaCl2 alone or associated with ethanol. Fasting blood Ca++ levels were not modified either by the secretin perfusion or by the intraduodenal CaCl2 infusion, either given alone or associated with ethanol.

Alkalies↗
PubMed1976

Evidences for duodenopancreatic reflexes and an anti-CCK factor with lidocaine infused intravenously and sprayed topically on pancreatic papilla in nonalcoholic and alcohol-fed dogs.

In 14 duodenal Thomas fistula dogs, four of them alcohol-fed for two years, lidocaine, applied topically to the duodenal pancreatic papilla, inhibited secretin-induced pancreatic secretion probably by interrupting duodenopancreatic reflexes that contribute to the "pancreon's" cholinergic tone. Opposite effects were observed with lidocaine administered against a CCK plus secretin background stimulation of the pancreas. The significant rising of volume and protein output above plateau levels were enhanced by chronic alcohol feeding. Lidocaine infused intravenously did not change secretin-induced pancreatic secretion but raised CCK and secretin evoked plateau secretion levels. Chronic alcoholism enhanced these latter effects. Atropine perfusion superimposed on CCK and secretin stimulation did not prevent but raised the intravenous lidocaine-induced pancreatic secretion changes. It is postulated that the modifications elicited by lidocaine sprayed topically and infused intravenously on CCK plus secretin evoked pancreatic secretion plateau levels are due to depression of an anti-CCK factor secreted by the small intestine mucosa.

Administration, Topical↗
PubMed1976

Reserpine-induced dissociation of canine pancreatic secretion.

In five dogs, provided with chronic pancreatic and gastric fistulas (Thomas' cannula), the effects on exocrine pancreatic secretion of an intravenous continuous perfusion of gastrin (Eurorga, hog gastrin I-II, 6 mug./kg./hr.) and secretin (GIH, 0.5 C.U./kg.hr.) was studied before and after 48 hours of reserpine treatment (0.1 mg./kg./24 hr.). When compared with the pretreated plateau levels, reserpine induced a significant pancreatic secretion dissociation, a depressive of the alkaline and a rising of the protein component. The former phenomenon suggests a participation of a catecholamines in the secretin-elicited pancreatic electrolyte secretion. The latter, an enhanced sensitivity of intranpancreatic and/or acinar cells of the "pancreon" to gastrin stimulation.

Animals↗