Biomedical subjects
O M Tiscornia
Publications and source records attributed to O M Tiscornia.
[Acute experimental pancreatitis in the opossum. The role of early splenectomy in the inflammatory response]].
BACKGROUND: The role of the Autonomous Nervous System in the immunologic and inflammatory response is still an issue of discussion. Furthermore, the physiopathologic mechanisms involved are still unknown. Acute pancreatitis (AP) does not escape this disconcert. In fact, like in every severe acute inflammatory process, its discontrol could be responsible of the high morbidity and mortality rates. OBJECTIVE: To assess to which degree bilateral splanchnicectomy changes the course of acute inflammatory response in AP. METHOD: Prospective research. RESULTS: The following parameters were evaluated: red blood cell count, white blood cell count, calcium, glucemia, urea, aminase, lypase and liver enzymes. Macroscopy and microscopy views of the pancreas were also obtained. The leucocitary response was abolished, and the calcium levels dropped to a lesser degree. CONCLUSIONS: Bilateral splanchnicectomy prior to unchaining AP had a beneficial effect, Its mechanism of action could have been through the disconnection of the respective reflex arches.
[Pseudo acute pancreatitis: a syndrome mimicked by a multiple parasitic duodenitis. Analysis of 7 case].
INTRODUCTION: The aim of this presentation was to analyze a clinical syndrome characterized by repeated episodes of upper abdominal pain, markedly increased levels of both total amylase and lipase, but with normal values of pancreatic isoamylase. Besides, with the lack of morphologic changes of the pancreatic gland, either by ultrasound, abdominal tomography, or Nuclear Magnetic Resonance. MATERIAL, METHODS AND RESULTS: Five female and two male patients, with an average age of 51 +/- 3 were studied. All had been diagnosed as having acute edematous pancreatitis (ranson score < 3). Laboratory tests had disclosed eosinophilia (5-30%); total amylasemia (1547 +/- 398 UA/l); lipasemia (857 +/- 499 UBL/L); normal pancreatic isoamylase (72 +/- 18 UA/L). Upper endoscopy showed nonspecific signs of duodenitis sometimes with duodenal erosions. Collection studies, pre and post Sorbitol, disclosed an unexpected multiple parasitic infestation, e.g.: giardias, ascaris, amoeba, hymenolepis nana. This finding was always suggestively associated with abundant sludge (bilirrubinate cholesterol and oxalate crystals). All patients, after having been submitted to the appropriate antiparasitic medication, were rapidly relieved of their symptoms and remained free of episodes of abdominal pain. CONCLUSIONS: When the fact that all our patients had normal pancreatic isoamylase levels and lack of any morphologic distortion of the pancreatic parenchyma is associated to the notion that total amylase and lipase may have as a source the gastrointestinal mucosa, it appears as a logical inference that the clinical syndrome here discussed is indeed primarily a reflection of an extrapancreatic disease, essentially of parasitic duodenitis.
[Acute experimental pancreatitis in the opossum. The role of prior truncular vagotomy on the inflammatory response].
BACKGROUND: Acute pancreatitis (AP) is a common cause of admission to the emergency room. Its etiopathogeny is poorly understood. The pancreatic inflammatory response in this process is unclear. The influence of the autonomic nervous system is a controversial issue. AIMS: To demonstrate the effects of truncular vagotomy on AP due to duodenal distention in the South American opossum. PLACE OF APPLICATION: Department of experimental surgery (Churruca-Visca Hospital) INEUCI (Neuroscience Institute, CONICET, UBA). POPULATION: Male and female South American opossum divided into: a control group (7 animals); group A: truncular vagotomy and pyloroplasty seven days after the onset of AP (7 animals). Group B: truncular vagotomy and pyloroplasty 30 days after provoking AP (7 animals). Group C: truncular vagotomy and pyloroplasty 45 days after the onset of AP (7 animals). METHODS: Acute pancreatitis was caused by duodenal distention of the second portion by inserting a Foley catheter through a gastrostomy. CONCLUSIONS: The method of provoking AP is original. The influence of autonomous nervous system is being underestimated in most of the literature available.
[Biliary acute pancreatitis: an etiopathology and evolution review of 148 cases].
BACKGROUND: A retrospective analysis of the etiologic factors and physiopathogenic mechanisms underlying an acute biliary pancreatitis episode put in evidence the complexity of the attempt to acquire a clear understanding of the entity. In this presentation the authors try to re-examine the main factors involved in the triggering of the disease. Besides the classic theories and their own approach to the management of an acute pancreatic inflammation episode are discussed. AIMS: The main purpose of this endeavor was to identify and discuss the etiopathogenic mechanisms that were prevalent in a series of 148 patients observed and treated in a 10 years period. Besides, another distinctive aim was to analyze their evolution and somehow to try to assess their probable prognosis. PLACE OF APPLICATION: Close community. POPULATION: The whole group of patients that were admitted with the diagnosis of acute pancreatitis in the time period comprised between 1987-1997. METHODS: The acute pancreatitis subgroups and their respective number of patient included were the following: BILIARY ACUTE PANCREATITIS 140 CASES POST ERCP 8 CASES CONCLUSIONS: As a result of the present reviewing endeavour several observations deserve to be pointed out: a. The pancreatic gland undoubtedly is a neuroendocrine organ, that is subjected to complex neural and hormonal influence. b. Undeniably, the involvement of the autonomic nervous system in the physiopathogenic mechanism of acute pancreatitis has been surprisingly disregarded. c. The biliary acute pancreatitis variant is the most frequent. What we consider a simplification is to accept the Opie's postulation without taking into account the intermediate steps, centered on autonomic reflexes, that ultimately lead to the acute inflammatory lesions. d. Although without an absolute proof, it is undeniable that "stress" is a primary etiology in some cases of acute pancreatitis. e. We favor the idea that the pancreas functional status influences on the extension and intensity degree of the acute pancreatic inflammatory lesions.
[Acute pancreatitis of uncommon etiology: a physiopathologic approach].
A review of 73 cases of acute pancreatitis (A.P.) of *A in frequent etiology is critically analyzed. The patients were allocated to the following categories: post ingestion of a large meal, dyslipemic, post ERCP, post operative, pregnancy, and puerperium linked., post urlian parotiditis, post stress, idiopathic, drug associated, post traumatic. In each of the above groups those hypotheses that are currently primarily accepted as been mainly concerned with the etiopathogenesis of the inflammatory episode were given preference. One factor upon which the authors has put special emphasis is that of frequent involvement of the nervous system through different types of autonomic are reflexes. This pathogenic mechanism is surprisingly disregarded in the literature. The interrelation ship between the severity of an AP episode and the background provided by the "pancreon" secretory activity is also emphasized. The mortality rate of the whole series was of 7 cases (9.6%). The groups that disclosed the highest rates were related to abdominal surgery (50%) and to dyslipemia (17%).
The effect of chronic intraperitoneal infusion of bacterial endotoxin on exocrine pancreas function in rats.
CONCLUSION: This study demonstrated that LPS infusion can induce tissue lesions and impair the exocrine protein secretion of the pancreas in rats. BACKGROUND: The effect of chronic ip infusion of lipopolysaccharide (LPS) on the exocrine pancreas function was studies in rats. METHODS: Four milligrams per kilogram per day of Salmonella typhi LPS were infused intraperitoneally by means of surgically implanted osmotic pumps. Rats were studied after 7-d LPS infusion. RESULTS: Plasma fibrinogen and amylase activity increased significantly in LPS-treated rats when compared with control rats. Histological examination of the pancreas showed congestion, infiltration, and focal necrosis in LPS-treated rats. The pancreas wet weight, as well as DNA and total soluble protein contents were significantly increased in LPS-treated animals when compared with controls. The pancreas protein output was significantly decreased in pure pancreatic juice, whereas the pancreatic juice flow rate was significantly increased in LPS-treated animals, when compared with controls. Electrophoretic patterns showed a marked decrease in digestive enzyme contents, whereas there was an increased content of 15 kDa protein.
A tribute to the memory of David A. Dreiling.
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Effect of ethanol intake on pancreatic exocrine secretion in mice.
Swiss mice were fed conventional lab chow and 10% ethanol or water as drinking fluid for 2 weeks. Pancreatic juice was obtained by cannulation of the bile pancreatic common duct of mice anesthetized with urethane. Isolated pancreatic lobules were also obtained. The flow rate and the amylase output were determined in pure pancreatic juice. The release of amylase was measured in pancreatic lobule preparations. The basal pancreatic juice flow rate and the amylase output were significantly increased by ethanol consumption. The magnitude of the pancreatic juice flow rate and the amylase output responses to increasing doses of bethanechol, a cholinergic agent, was significantly decreased in ethanol-fed mice. The amount of spontaneously released amylase was higher in pancreatic lobule preparations from ethanol-fed animals than that from control mice, and the difference was abolished by addition of atropine to the incubation media. The amylase release rate in response to increasing doses of bethanechol was significantly reduced in lobule preparations from the ethanol-fed group. These data indicate that ethanol intake in mice has a stimulating effect on the spontaneous pancreatic secretion and lends support to the hypothesis that ethanol consumption increases the intrapancreatic cholinergic tone.
Effects of intravenous ethanol on basal bile-pancreatic secretion in nonalcoholic and alcohol-fed rats.
In nonalcoholic (NA) and alcohol-fed rats (AF), intravenous-ethanol-induced percentage changes in bile-pancreatic-secretion (BPS) were evaluated, with and without gastric juice diversion (GJD) and with and without BPS duodenal recirculation (DR). Even with GJD, ethanol elicited a slight increase in BPS. These changes were greater in AF animals even when performed without GJD. When intravenous ethanol was given under conditions of GJD and DR, there were marked differences between the NA and AF animals in the ethanol-elicited post-plateau percentage changes of BPS. NA animals evidenced no significant difference from controls. But in the AF rats, ethanol triggered a marked and significant increase of flow, protein concentration, and output that became progressively greater in successive collection periods. It is postulated that without DR, and the resulting lack of negative duodeno-pancreatic reflexes (DPR), there occurs a change in reactivity to intravenous ethanol of the hypothalamic-bulbar nuclei (HBN) and in the mechanisms that modulate the flow of cholinergic impulses through the intrapancreatic ganglia (IPG). The postulated consequence is predominance (slight in NA rats receiving intravenous ethanol, greater in AF rats) in discharge of positive impulses from HBN and flowing unimpeded through the IPG to the "pancreon" units. In the NA animal with DR, ethanol may enhance BPS values, but in the AF rats, impairment of the negative DPR elicited by chronic alcohol intoxication might, after an acute intravenous ethanol injection, favor the discharge of positive impulses from the HBN flowing unimpeded through the IPG. In the AF rats also, ethanol would activate the nonnicotinic receptors of the neurons of the "antral," "duodenal," and "celiac" autonomic brains.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute pancreatitis in a patient treated for alcoholic hepatitis. The hypothesis of supranormal ecbolic stimulation of the pancreon.
A 33-yr-old white woman treated for alcoholic hepatitis developed acute pancreatitis during her hospital stay. At autopsy, two major pathological processes were found: alcoholic cirrhosis and chronic pancreatitis. In both, there was evidence of an acute episode, i.e., acute alcoholic hepatitis and acute hemorrhagic pancreatitis superimposed on the chronic alcoholic lesions. The sequence of events would indicate that the acute pancreatic pathology was precipitated by supranormal ecbolic stimulation of the acinar segment of the "pancreon" units, triggered as a result of a high protein and fat diet.
Pure pancreatic juice in humans: orange-lemon-juice-induced secretory effects. Comparative analysis with a regular meal, sorbitol, acidified peptone broth and secretin.
The secretory effect elicited by the ingestion of 100 ml of orange-lemon juice (O.-L.J.) was studied on pure pancreatic juice obtained from a catheter placed in the human Wirsung duct at surgery. These changes were compared with those evoked by a regular meal (R.M.), the ingestion of a Sorbitol solution (S.S.), the intragastric infusion of an acidified peptone broth (A.P.B.) and an i.v. single injection of secretin (Boots, 1.0 U/kg). The O.-L.J. induced purer pancreatic secretion response (flow, bicarbonate and enzyme output) than that triggered by the R.M., S.S. and A.P.B. The O.-L.J. evoked peak values, were observed earlier (60 min) than with a R.M. (90 min) ingestion. The 120-min-cumulative values confirmed these findings and disclosed that O.-L.J. elicits a rate of secretion and bicarbonate output closely similar to that of an i.v. secretin injection and amylase response greater than that evoked by this hormone. Thus, O.-L.J. ingestion proved to be an unexpected powerful stimulus of exocrine pancreatic secretion.
[Post-sectional antral peptic ulcer and antrofundic re-anastomosis in rats (manifestation of a probable antrofundic neuroendocrine center)].
The antrum-fundic section and re-anastomosis (AESR), liberates, in Wistar male rats, genuine antral peptic ulcers. They start within 20 days. They are progressive evolution, penetrating into all gastric walls. Between 7 and 8 months, they involve near organs (spleen, liver, pancreas) and produce a great inflammatory reaction of the peripancreatic ganglions. The antral peptic ulcer is induced if the gastric lesser curvature's nerves are sectioned and a concomitant pyloroplasty is done or not. The gastric hemisection, if anterior or posterior, break out the peptic ulcer only on the same side of the antrum-fundic interruption. In all this situations, except in cases of concomitant pyloroplasty, it is proved a pronounced and significantly increase of the gastric (g/kg), but not pancreatic index. In the AFSR series with nervous section on the lesser curvature and without pyloroplasty, the percentage of antral peptic ulcers in 56%. It is postulated the probably existence, at an antrum-fundic level, of a neuroendocrine center. Its nullification or disturbance by the section and re-anastomosis procedure could generate the antral ulcer and other histologic changes (increase of the "G" cells, hyperplasia of the parietal, ECL and "A like" cells) by one or various hypothetical ways: 1. Direct action, nullifying the normal blocking function of somatostative over the "G" cells and or parietal cells. 2. Disturbing or nullifying the motor pump effect of the gastric antrum, and on this way, enhancing the duodenum-gastric reflux with all know deleterious effects of the bile in the antrum particularly in an acid milieu. 3. Modifying, in the opposite direction, the sensitivity by one hand, of the "G" cells mass and by the other one, of the parietal, ECL and "A like" cells. The depression of the fundic sensitivity will induce the hyperplasia of the "G" cells, the hypersecretion of gastrin and, "a posteriori", all the secretory effects and trophic characteristic of it. 4. Disturbing the prostaglandins secretion, perhaps through a deficit of the nervous innervation, with the resulting epiphenomenon of a cytoprotection deficit mediated through the mucus and bicarbonate production. It is probably that the proposed physiopathogenic mechanism are associated and that the final result, the antral peptic ulcer is the consequence of an increase of the aggressive factors (acid, bile) and a concomitant depression of the defensive factors (cytoprotection), starting normally by the prostaglandins through the mucus and bicarbonate secretion.
[Acute pancreatitis: physiopathogenic hypothesis of fat necrosis].
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A laboratory preparation mimicking human peptic ulceration: a chronic antral peptic ulcer postsection and reanastomosis at the antral-fundic junction in the rat.
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Neural control of the exocrine pancreas: an analysis of the cholinergic, adrenergic, and peptidergic pathways and their positive and negative components. 2. Integration of neural and hormonal mechanisms.
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Neural control of the exocrine pancreas: an analysis of the cholinergic, adrenergic, and peptidergic pathways and their positive and negative components. 1: Neural mechanisms.
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Physiopathogenic hypothesis of alcoholic pancreatitis: supranormal ecbolic stimulation of the "pancreon" units secondary to the loss of the negative component of pancreas innervation.
In the rat, basal pancreatic secretion is generated and modulated by positive and negative duodeno-pancreatic reflexes. The former activates secretion, the latter acts as a "brake". Impairment of this brake plays a crucial role in the pathogenesis of alcoholic pancreatitis by causing elevation of pancreatic cholinergic tone and inducing increased pancreon ecbolic response to CCK-PZ stimulation. Both factors lead to pancreatic damage by supranormal stimulation of the pancreon.