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Biomedical subjects

R Laugier

Publications and source records attributed to R Laugier.

At least 73 records · Page 4Linked to original sources
PubMed1986

Exocrine pancreatic function of children from the Ivory Coast compared to French children. Effect of kwashiorkor.

One hundred nineteen children, either French or from the Ivory Coast, aged 1-8 years, were submitted to pancreatic function testing by duodenal aspiration. Trypsin, chymotrypsin, lipase, phospholipase, amylase, volume, bicarbonate, chloride, and calcium were estimated before and after an intravenous injection of 1 CU secretin + 3 CHR units pancreozymin per kilogram of body weight. Sixty-two patients were normal European children, and 11 were normal African children. Twenty-five African children presented with kwashiorkor and 10 African children had presented with kwashiorkor but had recovered at the time of the test. Three cases of recurrent kwashiorkor are also included. In the normal group of African children, phospholipase concentration, volume, and bicarbonate were significantly decreased but chymotrypsin and trypsin concentrations were not, when compared to the normal European population. In kwashiorkor patients, lipase, amylase, phospholipase, and chymotrypsin concentration were significantly decreased compared to normal Africans. Trypsin, volume, and bicarbonate were not affected. These modifications disappeared after refeeding. In cases of recurrent kwashiorkor, all enzymes, including trypsin, were decreased. Calcium was never modified. These modifications were very different from those observed in chronic alcoholic and hypercalcemic pancreatitis. In a two-year study, chronic calcifying pancreatitis (CCP) was diagnosed in 14 patients (13 males), hospitalized in Abidjan. The mean age at onset of the disease was 41 years (SD 12.71), which is very similar to European cases. The most frequent cause was alcoholism, as in Occidental countries. The nutrition of the population was low in protein, calories being provided mostly by manioc, but no apparent symptoms of malnutrition were observed in the parents of our patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Dopamine, noradrenaline and isoprenaline: secretory and electrophysiological effects in vitro on mouse pancreas.

The amylase release from mouse pancreatic fragments was studied after dopamine (DA), and alpha- or beta-sympathomimetic agonist application. The electrical parameters of the acinar cell membrane were also monitored. Both DA (from 5 X 10(-6) to 10(-4) M) and beta-stimulants (isoprenaline from 5 X 10(-6) to 5 X 10(-5) M; noradrenaline from 3 X 10(-4) to 10(-3) M) evoked an increase in amylase release, while noradrenaline in alpha-receptor stimulating doses failed to have any effect. The stimulatory effect of DA was blocked by ganglion blockers (Arfonad 10(-5) M; pentamethonium 3 X 10(-5) M) in a competitive manner and a dual antagonism was observed with atropine (10(-7) M, 10(-9) M). An alpha-receptor antagonist (phentolamine 10(-5) M) and a beta-receptor antagonist (propranolol 10(-5) M) had no influence on the dopamine response. Moreover, the DA-induced stimulation was dependent on the presence of extracellular calcium. Perfusion with 10(-4) and 10(-3) M-DA or local application (from 77 micrograms to 4.3 mg), resulted in marked membrane depolarization with diminution of the input resistance. This effect was blocked by atropine (10(-5) M) and pentamethonium (10(-4) M), but not by propranolol (10(-5) M) or phentolamine (10(-5) M). The isoprenaline- (IP) and noradrenaline- (NA) induced increase in amylase release was competitively blocked by propranolol (10(-5) M) but not by phentolamine (10(-5) M). Atropine caused a dose-dependent (10(-7) M, 10(-6) M) decrease in the maximal response (non-competitive antagonism), while the ganglion blocker pentamethonium (10(-4) M) was without effect. NA caused membrane depolarization accompanied by a decrease in the input resistance after local application (from 77 micrograms to 1.6 mg). This effect persisted in the presence of 10(-5) M-phentolamine but was abolished by 10(-5) M-propranolol. IP perfusion (10(-4) and 10(-3) M) or local application (0.3 M; from 32 to 130 micrograms) caused the same electrical changes as those induced by NA and DA. The effect of IP persisted in the presence of 10(-5) M-phentolamine, 10(-4) M-pentamethonium and 10(-4) M-domperidone, but was abolished by propranolol (10(-5) M) and tetrodotoxin (5 X 10(-6) M) and markedly diminished by atropine (10(-5) M).(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1985

Action of pirenzepine, a new muscarinic antagonist drug, on human pancreatic secretion.

The action of a new muscarinic antagonist drug on the pancreatic secretion has been studied in 12 healthy subjects. A stable pancreatic secretory plateau was obtained with submaximal hormonal stimulation (0.125 CU/kg/h secretin: 30 ng/kg/h caerulein). The highest dose of pirenzepine (40 mg) inhibited both volume and enzymatic concentration and output (-72.2% and -77.9% of plateau value for chymotrypsin and lipase output, respectively, 30 min after pirenzepine injection). The inhibition appeared immediately, lasted for more than 60 min, and was dose-related. The calcium dose-response curve paralleled those of lipase and chymotrypsin outputs. These results were comparable to those obtained with other anti-acetylcholine drugs and may be associated with the action of certain doses of ethanol on pancreatic secretion. In contrast, the lowest pirenzepine dose used (10 mg) induced a delayed stimulation of bicarbonate output, and bicarbonate concentration was not altered.

Adult↗
PubMed1985

Alcohol and the integrity of the pancreas.

Alcohol may affect the integrity of the pancreatic parenchyma, as seen in alcoholic pancreatitis, some cases of chronic alcoholism without clinical pancreatitis, and experimental studies. The composition of pancreatic juice may reflect some of these changes. One type of parenchymal alteration is the loss of differentiative features of acinar cells, so that they take on the characteristics of ductular cells. Concomitant fibrosis completes the formation of the tubular complexes found in association with alcoholic chronic pancreatitis. Sustained alcohol intake may produce the accumulation of lipid droplets in parenchymal cells, some of which may be shown to be within the rough endoplasmic reticulum of acinar cells. Epithelial cells may undergo mucous metaplasia. The epithelial-basal lamina barrier frequently is breached in the area of intraluminal aggregates, with or without obvious inflammation in the immediate area. Loss of barrier function may lead to interaction among components of the external compartment (lumen) and the internal compartment (stroma). Increased levels of blood proteins and glycosaminoglycans in the juice, enzyme activation, fibrin formation, and complement activation are potential consequences of barrier loss. Increased lactoferrin levels could result in part from the activity and degranulation of polymorphonuclear leukocytes.

Alcoholism↗
PubMed1985

The pancreas.

Explore the source record for details and available documents.

Adenocarcinoma↗
PubMed1983

Chronic obstructive pancreatitis after healing of a necrotic pseudocyst.

Seven patients presented with chronic pancreatitis localized upstream to a complete stenosis of the main pancreatic duct in its median part. This stenosis seemed to be secondary to the healing of a necrotic pseudocyst after either acute pancreatitis (four patients) or blunt abdominal trauma (three patients). In five patients, after spontaneous regression of the clinical symptoms of the initial pseudocyst, a silent period which ranged from 2 to 5 months was followed by recurrent attacks of pain of lesser intensity and shorter duration (less than 2 days) than observed during the evolution of the initial pseudocyst. These attacks of pain decreased spontaneously with time, probably because of the atrophy of the left part of the pancreas drained by the obstructed duct (in 6 months to 2.5 years). In 2 patients, the initial pseudocyst was revealed at the same time as the obstructive pancreatitis. The histologic features of chronic obstructive pancreatitis have been described. Fibrosis uniformly spread throughout the diseased pancreas with uniform atrophy of the exocrine parenchyma. Dilated ducts showed far less damages than in chronic calcifying pancreatitis. Since spontaneous clinical healing may be observed, surgical treatment is often useless. Only in patients with severe or frequent attacks is a Roux-Y anastomosis with the dilated part of the main pancreatic duct indicated rather than a risky left pancreatectomy.

Adult↗
PubMed1982

Effects of intravenous alcohol on pancreatic and biliary secretion in man.

Two groups of men, nonalcoholics (mean daily alcohol consumption less than 40 g) and alcoholics (mean daily alcohol consumption greater than 100 g) were compared with respect to the effects of intravenous ethanol on hormonally (secretin + CCK) submaximally stimulated pancreatic and bile secretion and chymotrypsin secretion during the basal state and after a Lundh test meal. Intravenous ethanol injection (600 mg/kg) significantly decreased pancreatic secretion of lipase (-74%), chymotrypsin (-78%), volume (-53%), and bicarbonate (-58%) in nonalcoholic but not in alcoholic men: The secretory pattern of the exocrine pancreatic response to an intravenous infusion of ethanol was therefore changes by the regular consumption of ethanol. The chymotrypsin concentration during the basal state was higher in alcoholic than in nonalcoholic men. This difference progressively disappeared after a test meal showing that chronic alcohol consumption modifies more basal than meal-stimulated pancreatic secretion.

Adult↗
PubMed1981

Ionic currents across pancreatic acinar cell membranes and their role in fluid secretion.

Fluid and enzyme secretion from a number of mammalian exocrine glands is controlled by the action of neurotransmitters and hormones on acinar cell membranes. Sustained stimulation evoking sustained fluid and enzyme secretion also evokes sustained membrane depolarization and increase in conductance. Mouse and rat pancreatic fluid and enzyme secretion, as well as membrane depolarization and conductance increase evoked by sustained stimulation with acetylcholine or cholecystokinin-gastrin peptides, are acutely dependent on extracellular calcium. However, the initial stimulant-evoked conductance increase and secretion appear to be triggered by calcium released from inside the cells. Direct measurement of membrane current during sustained stimulation in voltage-clamp experiments with resolution of the total current into its Na, Cl and K components has allowed calculations of stimulant-evoked Na and Cl uptake into the acinar cells. The NaCl uptake is quantitatively sufficient to account for the stimulant-evoked fluid secretion. The role of the stimulant-evoked transmembrane ionic current appears to be the supply of salt for the fluid secretion. Calcium derived from intracellular sources in the initial phase of secretion, and from the extracellular fluid in the sustained phase, couples fluid and enzyme secretion to hormone-receptor interaction.

Bicarbonates↗
PubMed1981

Two different types of electrogenic amino acid action on pancreatic acinar cells.

The electrogenic action of the basic amino acid, L-arginine, has been compared with the action of the neutral amino acids, L-alanine and glycine, in mouse pancreatic acinar cells. All three amino acids cause membrane depolarization, but while the reversal potential for the action of the neutral amino acids is close to the calculated value of the Na equilibrium potential (+30 mV) the reversal potential for the L-arginine effects is +7 mV. The neutral amino acids exhibit mutual inhibition, but L-arginine did not inhibit the L-alanine- or glycine-evoked depolarization nor did the neutral amino acids inhibit the action of L-arginine. While L-alanine markedly depressed acetylcholine-evoked depolarization, L-arginine had no such effect. It is concluded that there are at least two quite different types of electrogenic amino acid action in pancreatic acinar cells.

Acetylcholine↗
PubMed1981

Alcoholic pancreatitis.

Although further work is needed for understanding the mechanism of the action of alcohol on the pancreas, it can be admitted that in man, the rat and the dog, chronic alcohol consumption leads to precipitation of proteins in the juice and the ducts. When these precipitates are observed, an alteration of the protein to bicarbonate ratio is always found, as a result of an increase in protein concentration or a decrease in bicarbonate concentration, or both, It is reasonable to assume that an increased cholinergic tone is responsible for the increased secretion of protein. The decrease in bicarbonate secretion is not explained. It is worthwhile mentioning that, in hypercalcaemic dogs, protein precipitates are found in the juice associated with an increased concentration of protein and a decreased concentration of bicarbonate. It is known that hypercalcaemia (hyperparathyroidism) is a cause of chronic calcifying pancreatitis (noel-Jorand et al, 1981b).

Alcoholism↗