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Biomedical subjects

H Sarles

Publications and source records attributed to H Sarles.

At least 109 records · Page 6Linked to original sources
PubMed1986

Effect of atropine on pancreatic secretion in conscious rats.

The effect of atropine on exocrine pancreatic secretion was investigated in conscious rats. Intravenous atropine infusion decreased nonstimulated protein secretion during recirculation of pancreatic juice into the duodenum D50 = 15-20 micrograms/kg/h. The maximum inhibition from protein secretion (-89%) was obtained with 600 micrograms/kg/h. With larger doses, the inhibition was less. The response to secretin and cholecystokinin-pancreozymin was not significantly modified by atropine. When pancreatic juice was diverted during the course of an intravenous atropine infusion, the first 1-hour peak of protein output was significantly decreased, but the following 2-hour period was increased, the sum of these 2 periods being similar in both conditions. The response to soybean trypsin inhibitor during recirculation was decreased as well as the first peak after diversion. During atropine infusion fluid secretion decreased more powerfully after 1 h diversion and after soybean trypsin inhibitor than during recirculation of pancreatic juice. It is suggested that during recirculation of pancreatic juice nonstimulated protein secretion is mostly (89%), and water secretion is partially controlled by cholinergic mechanisms. After soybean trypsin inhibitor stimulus and during the early phase following juice diversion protein secretion seems to be partly under the control of cholinergic mechanisms. However, during the latter phase following diversion, it is not so. Parasympathetic stimulation appears also to play a significant, although less important, role in fluid secretion.

Animals↗
PubMed1986

Localized necrohemorrhagic pancreatitis in the rat after pancreatic interstitial trypsin injection. Regressive pseudochronic lesions.

Different materials dissolved in 0.9% NaCl were injected into the connective, interlobular tissue of the duodenal part of the rat pancreas. Activated rat pancreatic juice or trypsin were able to induce localized necrohemorrhagic pancreatitis. Only mild edema and leukocytic infiltration were observed after injecting bovine albumin, chinese ink, trypsinogen or nonactivated pancreatic juice. The progression of histological changes was followed for 2 weeks in the trypsin-induced pancreatitis. Limited foci of severe hemorrhage, liquefaction and coagulative necrosis were observed in the first 24 h. Acinar cell degeneration and regeneration were observed 48 h after the operation, fibroblasts appearing in the interlobular spaces. Four days after injection, inter- and intralobular fibrosis, acinar cell degeneration and tubular complexes were observed, presenting a picture characteristic of chronic pancreatitis. Some minimal changes were still seen in the pancreas 1 week after injection, but by the end of the 2nd week the pancreatic histology was normal. These results demonstrate the significance of active trypsin in the pancreatic interstitium with respect to the induction of pancreatitis. This model of localized necrohemorrhagic pancreatitis is highly reproducible and without significant mortality. Following the acute process, histological changes resembling chronic pancreatitis can be observed, but they are completely reversible.

Acute Disease↗
PubMed1986

[Intra-epithelial carcinoma of the pancreas. Study of a case and review of the literature].

The authors report the case of a 74 year-old woman who was hospitalized for severe abdominal pain. The patient had epigastralgia for many years. Biology revealed hyperamylasemia and computerized tomodensitometry showed that the pancreas head was enlarged. At retrograde wirsungography a short stenosis was visible in the pancreatic duct, 2 cm from the papilla. This was considered to be a tumor and surgery was performed. Histological sections of the pancreatic head showed strictly intraductal carcinoma "de novo" or associated with ductal epithelial hyperplasia. Although very rare, in situ carcinoma should be considered when clinical features are unexplained in order to perform radical surgery.

Aged↗
PubMed1985

[Chronic calcifying pancreatitis, pancreatic calculi. New data].

There are two different forms of chronic pancreatitis: one is obstructive pancreatitis which results from a pre-existing obstacle (usually a tumour or a scar) and the other, much more frequent, is chronic calcifying pancreatitis which seems to begin with the formation of precipitates in acini and ducts, later transformed into stones and calcifications made up of calcium carbonate, and therefore is a pancreatic lithiasis. Since the pancreatic juice is supersaturated in calcium carbonate, the presence of an inhibitor of crystallization must be postulated. This has now been identified as a 13500 daltons molecular weight protein: the pancreatic stone protein secreted by the acinar cells. This protein is decreased in chronic calcifying pancreatitis irrespective of its origin (alcoholic, hereditary, hypercalcaemic, tropical, idiopathic), although its reduction is unrelated to any of these aetiological factors. Chronic alcohol consumption may encourage calcium stone formation possibly by disturbing the cholinergic regulation of pancreatic secretion, with decrease in citrate secretion (citrate is a chelator of calcium) and increase in enzyme secretion. The diagnostic and therapeutic implications of these findings are already obvious.

Alcoholism↗
PubMed1985

Nutritional data and etiology of chronic pancreatitis in Mexico.

Alcoholism and malnutrition have been implicated commonly in the etiology of chronic pancreatitis (CP). The geographical distribution and clinical and nutritional features differ between the alcoholic and tropical forms of CP. This work presents the etiology and nutritional characteristics of CP in Mexico, a country in which both alcoholism and childhood malnutrition are common. Two well-defined groups of patients have been identified: an alcoholic group composed mainly of males with a mean age at clinical onset of 41 years and a high dietary intake of fat, protein, carbohydrates, and calories; and a nonalcoholic group with a female preponderance, a mean age at onset of 23 years, and a higher intake of protein than controls. We conclude that alcoholic chronic pancreatitis in Mexico is similar to that reported in other temperate countries. Although the nonalcoholic group resembles that observed in tropical countries in many ways, our patients are not malnourished, further questioning the role of childhood malnutrition in the pathogenesis of this type of chronic pancreatitis.

Adolescent↗
PubMed1985

Evaluation of Angelchik antireflux prosthesis. Long-term results.

Fifteen patients with intractable reflux or its complications were sequentially studied after the placement of the Angelchik antireflux prosthesis. In all, 16 devices were inserted. Parameters were measured before and 3, 12, 24, and 36 months after prosthesis placement and included symptom scoring, esophageal manometry with Tuttle test, endoscopy, suction biopsy, barium swallow, and gastroesophageal scintigraphy. In addition, a subset of patients underwent stimulation/inhibition of the lower esophageal sphincter (LES) with pentagastrin, metoclopramide, edrophonium, and atropine. At a mean time of 16 months postsurgery, 10 of 16 (63%) patients were reflux-free and there was significant improvement in endoscopic, biopsy, and symptom scoring. Post-insertion, there were statistically significant increments in LES pressure with intravenous boluses of pentagastrin, metoclopramide, and edrophonium, and a significant decrease with atropine. Two patients who developed prosthesis herniation into the chest required removal because of ongoing reflux and dysphagia. An additional patient had prosthesis disruption and migration, which also required removal. Four patients with previously failed antireflux procedures had five prostheses placed. All continued to reflux postoperatively. No patient who was initially reflux-free subsequently developed reflux, despite a tendency for LES pressure to decline with time. Although this procedure proved effective for up to 36 months in patients who had had no previous antireflux procedure, the displacement rate (3/16 = 19%), reoperation rate (3/16 = 19%), and the progressive decline in LES pressure over time should make one cautious about its routine use in the surgical treatment of reflux esophagitis.

Endoscopy↗
PubMed1985

Pancreatic stone protein. I. Evidence that it is encoded by a pancreatic messenger ribonucleic acid.

We have previously shown that the pancreatic stone protein (PSP) is an inhibitor of calcium carbonate crystal growth and may participate in the stabilization of the normally supersaturated pancreatic juice. Our aim in this study was to determine if PSP is a normal secretory product of the human pancreas by determining if the normal human pancreas contains a messenger RNA coding for PSP. Human pancreatic messenger RNAs were used to direct protein synthesis in a cell-free translation system. Immunoprecipitation of translation products with a monospecific antibody directed against the PSP yielded a product migrating as a single homogeneous band on sodium dodecyl sulfate-polyacrylamide gels. This product has a molecular weight of 16,000, the value expected for pre-PSP. Products selected by immunoprecipitation with antitrypsin-1 antibodies also migrated as a single band, with a molecular weight of 27,000. It is concluded that a messenger RNA coding for pre-PSP, distinct from the messenger RNA coding for pretrypsinogen, is present in human pancreas. These results support the hypothesis that PSP is a molecular entity, and not a degradation product of trypsinogen 1 or another pancreatic protein.

Animals↗
PubMed1985

Pancreatic stone protein. II. Implication in stone formation during the course of chronic calcifying pancreatitis.

Pancreatic stone protein, a novel protein isolated from pancreatic stones of patients suffering from chronic calcifying pancreatitis and secreted in normal human pancreatic juice, was measured by radial immunodiffusion in pure pancreatic juice. Patients with chronic calcifying pancreatitis of different etiologies had significantly lower levels of pancreatic stone protein when compared with other pancreatic diseases and controls. Pancreatic stone protein suppresses in vitro calcium carbonate precipitation and therefore stabilizes normally supersaturated pancreatic juice. The decreased pancreatic stone protein levels observed could be a key factor in the growth of calcium carbonate crystals and stone development during the course of chronic calcifying pancreatitis.

Adolescent↗
PubMed1985

Entero-pancreatic reflexes revealed by duodenal anesthesia in the dog.

This study was designed to improve our understanding of duodeno-pancreatic reflexes, the existence of which was suggested by the previous observation of a reduction in secretin-stimulated pancreatic secretion during local anesthesia of the duodenal mucosa. The effects on this reduction in secretin-stimulated secretion of cholinergic or adrenergic blocking agents (alone or in combination) and of truncal vagotomy, were studied in conscious dog with gastric and pancreatic fistulae. For each agent and for secretin alone in normal and vagotomized dogs, a comparison was made of pancreatic secretion with and without lignocaine anesthesia of the duodenal mucosa. Lignocaine reduced pancreatic secretion with secretin alone, and stimulated it during infusion of atropine. The changes in both protein bicarbonate secretion were blocked by pentolinium and by phenoxybenzamine whereas propranolol mainly blocked the effects on bicarbonate output. The effect of truncal vagotomy resembled that of atropine. These results suggest the existence of two enteropancreatic reflex mechanisms; an excitory cholinergic vagal reflex and an inhibitory, atropine-resistant non-vagal reflex. Both are blocked by pentolinium (a ganglion blocker) and by phenoxy-benzamine, suggesting the involvement of alpha-adrenergic receptors probably also at the level of the ganglion cell. Beta-adrenergic receptors are also involved in the regulation of bicarbonate and fluid secretion.

Anesthesia↗
PubMed1985

Citrate and calcium secretion in the pure human pancreatic juice of alcoholic and nonalcoholic men and of chronic pancreatitis patients.

Citrate, calcium and protein have been estimated in pure pancreatic juice after a secretin and a CCK injection in 4 patients presenting with alcoholic calcified pancreatitis (ACP), 10 controls without evidence of pancreatic disease, drinking more than 130 g alcohol/day, and 10 controls without evidence of pancreatic disease, drinking less than 20 g alcohol/day. Citrate is normally secreted in the pancreatic juice and this secretion increases in parallel with protein after CCK injection. Citrate secretion is significantly decreased in the two alcoholic groups. Calcium secretion is increased in the ACP, and reasons are presented to suggest that this may be due to lesions of the ducts. These modifications could play a role in the formation of pancreatic stones which are mostly built up of calcium carbonate.

Alcoholism↗
PubMed1985

Effect of acute and chronic oral administration of ethanol on canine exocrine pancreatic secretion.

The action of an intragastric injection of ethanol (1.0-1.5 g/kg), either in the fasting animal or with a solid meal, has been studied in two groups of 4 conscious dogs provided with gastric and duodenal Thomas cannulae: one group of 'alcoholic dogs' (AD) had been given 2 g/kg/day ethanol over a period of 24 months, the second group of 'nonalcoholic dogs' (NA) had been given water as control. In NA, intragastric ethanol inhibited water and bicarbonate secretions, alcohol being given in the fasting animal or with a meal. In AD: (a) the nonstimulated output of water and bicarbonate, and to a lesser extent of protein, was decreased compared to NA, protein concentration being increased; (b) the bicarbonate response to a meal without ethanol was decreased, and (c) the most interesting finding is that in AD, the inhibitory action of intragastric ethanol as observed in NA, disappeared and was even replaced by a stimulation of water, bicarbonate and protein secretions. The disappearance in AD of alcohol-induced mechanisms inhibiting pancreatic secretion had already been found with other experimental protocols and involves muscarinic receptors. Inhibition of water and bicarbonate secretions remains unexplained.

Administration, Oral↗
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↗