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Biomedical subjects

H Sarles

Publications and source records attributed to H Sarles.

At least 199 records · Page 11Linked to original sources
PubMed1980

Chronic ethanol consumption and exocrine pancreatic response to ethanol and acetaldehyde in the rat.

The action of ethanol and acetaldehyde on exocrine pancreatic secretion of a group of normal and a group of chronic (18 months) alcohol-fed Sprague-Dawley rats were investigated. The volume of basal pancreatic secretion was significantly larger in alcoholic rats, but in contrary to previous studies the response to acute intravenous, intragastric and intraduodenal ethanol administration was not significantly different in the two groups. Intragastric and intraduodenal ethanol stimulated both volume and protein secretion, but intragastric ethanol did not stimulate pancreatic secretion after pyloric ligation. Only high doses of intravenous ethanol (4 g/kg but not 2 g/kg) on inhibited pancreatic secretion. Pharmacological intravenous doses of acetaldehyde (500 mg/kg/h) inhibited fluid and protein secretion but 100 mg/kg/h was without effect. This shows that the response of the rat pancreas to alcohol and acetaldehyde is different from the response of dogs and men.

Acetaldehyde↗
PubMed1980

Jaundice and chronic pancreatitis.

A study was conducted on a group of 48 patients presenting with jaundice during the course of chronic pancreatitis. Two different patterns of symptoms could be opposed: (1) Short-lasting cholestatic jaundice which is accompanied by pain, but free from pruritus and fever, is linked to a medium consumption of alcohol, occurs in the course of advanced chronic pancreatitis and seems to be the consequence of a stricture of the main bile duct due to pancreatic lesions. (2) Protracted, intense jaundice which is linked to a high alcohol consumption, is encountered among less-advanced cases of chronic pancreatitis, the main bile duct being generally normal. In such a case, direct toxic effect of alcohol on the liver must be questioned.

Alcohol Drinking↗
PubMed1980

The effect of acetaldehyde on pancreatic and gastric secretion.

To ascertain whether any of the well-known effects of intravenous ethanol on pancreatic and gastric secretion could be due to its metabolite--acetaldehyde, a strong cytotoxic and sympathomimetic agent--acetaldehyde was given intravenously for 1 h (50, 100, and 200 mg/kg/h) in seven dogs. Acetaldehyde did not modify pancreatic secretion stimulated with secretin and caerulein, but under basal conditions 200 mg/kg/h slightly increased the volume and protein content of pancreatic juice. Acetaldehyde increased gastric secretion up to 4.03 meq/15 min in a dose-dependent manner, while serum gastrin remained unchanged. The increase of acidity persisted after propranolol and was inhibited but not abolished by ganglionic blockade. It can be concluded that physiological concentrations of acetaldehyde do not interfere with pancreatic secretion and that it is possible that the stimulatory effect of ethanol on gastric secretion is mediated at least partly through acetaldehyde.

Acetaldehyde↗
PubMed1980

Dose-related inhibition of gastric secretion by intraduodenal trypsinogen in dogs.

It has been shown previously that trypsinogen and its activation peptide but not trypsin decreased gastric secretion. The purpose of this work was to study the dose-action relation between the intraduodenal infusion of trypsinogen and gastric secretion. Three dogs provided with gastric and duodenal Thomas fistulae were stimulated by continuous i.v. perfusion of porcine gastrin I-II (6 microgram kg-1 h-1). Pancreatic juice was diverted to the exterior and gastric secretion was collected. Upon reaching a gastric secretory plateau, porcine trypsinogen was infused intraduodenally at doses of 5, 10, 20, 40, 80 and 160 mg. Each test was continued for a further 60 min. Control was made with isotonic saline. There was a dose-related inhibition of the gastrin-stimulated gastric acid output. This inhibition reached a maximum of 50% with 40 mg of intraduodenal trypsinogen, showing no increase with higher doses.

Animals↗
PubMed1980

Inhibition of exocrine pancreatic secretion by alpha-adrenergic blocking agents in conscious rats.

The effects of the alpha-adrenergic blocking agents, phentolamine and phenoxybenzamine were tested on the exocrine pancreatic secretion of conscious rats. Phentolamine (0.156 mg/kg to 1.25 mg/kg) and phenoxybenzamine (1.25 and 2.5 mg/kg) strongly inhibited basal volume and protein secretion. On the other hand, phentolamine had no effect on the cholecystokinin-pancreozymin or urecholine stimulated exocrine pancreatic secretion. The infusion of phentolamine (1.25 mg/kg/hr) greatly impaired the stimulatory effect on protein secretion induced by soybean trypsin inhibitor and oleic acid. These experiments suggest that alpha-adrenergic blocking agents inhibit pancreatic secretion of the conscious rat by impairment of cholecystokinin-pancreozymin release either by a direct inhibitory action or by blocking a still unknown alpha-adrenergic stimulatory reflex present in the duodenal mucosa.

Adrenergic alpha-Antagonists↗
PubMed1980

Effect of atropine on different phases of pancreatic secretion in conscious rats.

The effect of submaximal doses of intravenous atropine and their combination with topical anaesthesia of the intestine by oxethazaine-HCl was investigated in conscious rats. I. Basal water, bicarbonate and protein secretion were significantly augmented after diversion of pancreatic juice. On the basis of the protein secretory pattern of basal secretion, 2 stable stages have been recognized: 1. The most physiological basal stage during return of pancreatic juice. 2. The first, highly elevated plateau from the 4th to the 7th 30 min period after diversion. 3. The second delayed and less elevated plateau after 240 min diversion. II. Atropine greatly suppressed protein secretion during recirculation but only moderately after diversion of juice, and during the first plateau an atropine resistant peak appeared. Inhibition of water secretion was equal during all the stages. Atropine infusion resulted in a further decrease in pancreatic secretion also after topical anaesthesia of the intestine. It was concluded that atropine had a complex effect on pancreatic secretion: it possibly decreased the CCK release in the first period after diversion but not later, and decreased the duodenopancreatic reflexes and other factors of the cholinergic tone.

Animals↗
PubMed1980

Action of catecholamines on exocrine pancreatic secretion of conscious rats.

The effect of four different catecholamines (adrenaline, noradrenaline, isoprenaline and dopamine) were tested on the exocrine pancreatic secretion of conscious rats equipped with a pancreatic and biliary fistula, bile being continuously recirculated into the duodenum. Contrary to what has been observed in the anaesthetized animal neither of these four catecholamines had any stimulatory effect on volume. High bolus doses of adrenaline (440 microgram/kg) or noradrenaline (80 microgram/kg) or dopamine (10 mg/kg) inhibited volume and protein secretion probably by inducing strong vasoconstriction and anoxia. The infusion of high doses of dopamine (2.5 mg/kg/hr) induced a significant inhibition of volume and protein output. This inhibitory effect was neither modified by propranolol nor by haloperidol proving that it was a non specific effect secondary to the increase of vascular resistence. Isoprenaline either injected (125, 250 and 500 microgram/kg) or infused (25 microgram/kg/hr) induced an inhibition which was blocked by propranolol. It is suggested that in conscious rats, circulating catecholamines have probably a limited role in the control of pancreatic secretion although they could have some inhibitory action on protein secretion. Isoprenaline inhibits protein secretion probably by acting on a beta receptor mechanism. The pancreas of the rat does not seem to have stimulatory dopamine receptors.

Animals↗
PubMed1979

Exogenous and endogenous stimulations during different phases of pancreatic secretion in conscious rats.

The effects of stepwise increasing doses of intravenous caerulein, secretin, urecholine and intraduodenal oleic acid were investigated in conscious rats. a) Basal water, bicarbonate, and protein secretion significantly augmented after diversion of pancreatic juice. On the basis of protein secretory pattern of basal secretion 3 stable stages have been recognised: 1. The most physiological basal stage during return of pancreatic juice. 2. The first, highly elevated plateau from the 4th to 7th 30-min period after diversion of pancreatic juice. 3. The second, delayed and less elevated plateau after 270 min. b) The following patterns of stimulated secretion were observed: 1. Caerulein stimulated protein and bicarbonate secretion during return of juice and the first plateau but it failed to elicit a significant response during the second, delayed plateau. 2. Secretin and urecholine showed similar protein responses during return of pancreatic juice but after diversion, they stimulated water and bicarbonate secretion only. 3. During the second plateau oleic acid stimulation resulted in a significant increase in water and bicarbonate secretion but no significant increase occured in protein output. The delayed inhibition of protein secretion, previously described in our laboratory, was unchanged. 4. Supramaximal doses of exogenous stimuli caused an inhibition in pancreatic secretion.

Animals↗
PubMed1979

Inhibition of rat basal pancreatic secretion by intraduodenal bile.

The effect on basal exocrine pancreatic secretion of diversion from and reintroduction into the duodenum of bile has been studied on conscious rats provided with pancreatic, biliary and duodenal fistulae. Diversion of bile from the intestine augmented protein output by 30%. After an eight-hour diversion recirculation of bile into the duodenum reduced pancreatic protein output by 30%; volume being not significantly modified. When either bile was diverted or the main bile duct was ligated, a similar inhibition of protein secretion was observed after intraduodenal injections of 20 mM solutions of taurocholate, taurochenodeoxycholate, chenodeoxycholate, and cholate, and of synthetic mixed micelles (bile salts, lecithin). Inhibitory action of bile salts on pancreatic secretion was seen equally whether or not the bile salts were in free or conjugated form or pancreatic juice returned to the intestine. We conclude that unlike man and the dog, bile as well as pancreatic juice inhibits the basal pancreatic exocrine secretion of the rat.

Animals↗
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

[Interaction of dimethyl prostaglandin E2 and ethanol on the pancreatic secretion of the rat].

We have studied the action of 16,16-dimethyl prostaglandin E2 methyl ester (DiMePGE2) on pancreatic secretion in the unanesthetized rat with pancreatic and duodenal fistulae. DiMePGE2 inhibited volume, protein secretion and bicarbonate output. The inhibition of protein concentration is dose related (ED50 = 5.35 microgram/rat). DiMePGE2 was effective by the intraduodenal, intravenous, and intraperitoneal routes. Intraduodenal infusion of ethanol alone (2 mL 16% (v/v) in 1 h) strongly increased protein secretion (concentration, +30%; output, +69%) When 4 microgram DiMePGE2 was injected intraperitoneally just before the ethanol infusion, the secretory effect of ethanol disappeared and the inhibition was similar to that observed with DiMePGE2 alone.

Animals↗
PubMed1979

Cyclic nucleotides, calcium, bicarbonate, and protein secretion in canine pancreatic juice in response to cholecystokinin-pancreozymin.

The secretion of cyclic AMP, cyclic GMP, protein, calcium, and bicarbonate in the pancreatic juice of three nonanesthetized dogs with chronic gastric and duodenal Thomas cannulae has been studied. Intravenous infusions of increasing doses of cholecystokinin-pancreozymin (CCK) (1.5, 3, 6, 12, 24 Crick Harper-Raper (CHR) U kg-1 h-1) were administered together with a continuous submaximal dose of secretin (1 clinical unit (CU) kg-1 h-1). Doubling CCK doses every 45 min induced a parallel increase in the output of both cyclic nucleotides. Cyclic AMP output peaked at between 15 and 30 min for 3 and 6 U kg-1 h-1 of CCK and later for 12 and 24 U kg-1 h-1 of CCK whereas cyclic GMP output increased more constantly. Calcium output followed a pattern similar to that of cyclic GMP secretion. Flow rate and protein output attained their peaks at between 30 and 45 min. A strong linear correlation was found between the quantities of cyclic AMP, cyclic GMP, and the quantities of protein secreted in response to each CCK dose. This study demonstrates the presence of cyclic GMP in the canine pancreatic juice and the dose-dependent stimulation of the secretion of cyclic GMP and cyclic AMP by CCK in the presence of secretin.

Animals↗
PubMed1979

A multicenter inquiry into the etiology of pancreatic diseases.

A multicenter study on the etiology and diet of patients with pancreatic diseases has been realized with the collaboration of 36 centers in 19 countries having widely different climatic and racial conditions. 2,478 cases were studied: acute pancreatitis (AP), 222 males, 208 females; calcified chronic pancreatitis (CCP), 801 males, 134 females; non-calcified chronic pancreatitis (NCCP), 525 males, 155 females; pancreatic cancer (PK), 69 males, 14 females; controls, 281 males, 62 females. The analysis of mutual information and the factorial analysis of correspondences have been used. With regard to chronic pancreatitis, the 19 countries could be classified into 4 classes presenting relative similarities. (A) Southern Europe: The diet is rich in carbohydrates, protein and lipids, alcohol intake is primarily in the form of wine and the pathology is dominated by CCP. There are much fewer women than men with chronic pancreatitis. (B) Northern Europe, to which may be added Argentina and Chile, is characterized by a protein- and lipid-rich diet, a beer-based alcohol consumption and a distinct prevalence of AP and NCCP. The prevalence of males with chronic pancreatitis is less marked than in southern Europe. (C) Japan has a lipid-poor diet and a low frequency of CCP and NCCP. (D) A fourth group is mostly composed of tropical countries with mixed races. It may be divided into 2 subclasses: (a) India is the most characteristic country of the first type with low fat, low protein diet, no alcoholism, high frequency of CCP (at an early age); (b) Brasil and South Africa are representative of the second subclass with very high alcohol intake in the form of spirits and a high frequency of CCP.

Adult↗