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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper attempts to demonstrate the influence of gallstones, from different locations, on ultrastructural changes in pancreatic acinar cells. Forty-two gallstone patients with no record of clinical pancreatitis are the subjects of this study. Of these patients, 14 have cholecystolithiasis, 14 have choledocholithiasis, and 14 have primary hepatolithiasis. The findings reveal the following ultrastructural alterations of the pancreatic acinar cells: dilation of the rough endoplasmic reticulum, accumulation of lipid droplets, an increase of autophagic vacuoles, residual bodies and myelin figures, alteration of electron density of zymogen granules, and alteration of mitochondria. All these ultrastructural changes are similar to those of clinical acute pancreatitis. With three locations of calculi, these different kinds of gallstones have a similar affect on the fine structure of pancreatic acinar cells, and these changes occur regardless of the size of the common bile duct and the biochemical data. This suggests that irrespective of the location of the gallstones, subclinical cellular injury to acinar cells is caused.
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PMID:Effect of gallstones on pancreatic acinar cells. An ultrastructural study. 322 32

Rats infused with a dose of the secretagogue caerulein that is in excess of that which stimulates a maximal rate of pancreatic digestive enzyme secretion develop acute edematous pancreatitis. We have previously noted that infusion of this dose of caerulein (5 micrograms . kg-1 . h-1) induces the appearance of large heterogeneous vacuoles in acinar cell, blockade of exocytosis, and intracellular accumulation of digestive zymogens [O. Watanabe et al. Am. J. Physiol. 246 (Gastrointest. Liver Physiol. 9): G457-G467, 1984 and A. Saluja et al. Am. J. Physiol. 249 (Gastrointest. Liver Physiol. 12): G702-G710, 1985]. The current studies were performed to further elucidate these phenomena at the electron microscopic level of resolution and employed the techniques of pulse labeling, radioautography, and immunolocalization. Rats were infused with caerulein (5 micrograms . kg-1 . h-1) for 1 h, given a pulse of [3H]phenylalanine, and killed at selected times during the subsequent 5- to 180-min postpulse period during which caerulein infusion was continued. Transport from the endoplasmic reticulum to the Golgi cisternae was not altered by supramaximal stimulation, but transport through post-Golgi elements was altered. In particular, the maturation of condensing vacuoles into zymogen granules was found to be impaired. This led to the accumulation of partially condensed vacuoles and to the development of the large vacuoles containing newly synthesized digestive zymogens as well as the lysosomal hydrolase cathepsin D. The source of the latter could be impaired sorting of lysosomal and digestive enzymes and/or fusion of vacuoles with lysosomes. At the later times after pulse labeling, mature zymogen granules were also found to fuse with these large cathepsin D-containing vacuoles by a process analogous to crinophagy. Thus these studies indicate that the large heterogeneous vacuoles that appear during supramaximal secretagogue stimulation and that contain admixed digestive zymogens and lysosomal hydrolases arise by at least two mechanisms, impaired condensing vacuole maturation and crinophagy.
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PMID:Intracellular transport of pancreatic zymogens during caerulein supramaximal stimulation. 366 11

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.
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PMID:Alcohol and the integrity of the pancreas. 385 12

Human pancreas tissue was studied electron microscopically during various stages of shock. The subcellular changes of exocrine pancreas affect in particular endoplasmic reticulum (ER), mitochondria, cytoplasm, and nuclei. Alterations correlate with duration and severity of shock, causing cell death in prolonged or severe manifestations of shock. This is obviously due to release of enzymes from zymogen granules; the ensuing damage cannot be distinguished from autodigestive pancreatitis. Lesions of exocrine pancreas cells are of multifactorial origin, arising from general shock-induced hypoxia, but also from local ischemia due to disturbed microcirculation provoking intravasal coagulation. Beyond these main causes, intracellular disorders of metabolism, obstruction of lymph drainage, and nervous factors may be of influence. As the cases surveyed in this paper had no fatal outcome - except for one patient - the changes described can be defined as non-lethal or as reversible.
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PMID:Ultrastructural changes of the human pancreas in acute shock. 402 38

Staphylococcal alpha-toxin induced pancreatitis in dogs was studied by electron microscopy. Pancreatic acinar cell injury was indicated by increased vesiculation of endoplasmic reticulum, loss of intracisternal granules, changes in mitochondria, membrane discontinuities and an increased number of dense complex bodies, lipid droplets and free ribosomes.
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PMID:Effect of staphylococcal alpha-toxin on the fine structure of pancreatic acinar cells of dogs. 433 16

The aim of the present study was to determine the effect of prolonged ethanol intake on the morphology and protein metabolism in the rat pancreatic acinar cells. Weight-matched triplets of Sprague-Dawley rats were fed Lieber-DeCarli diet containing 5% (wt/vol) concentration of ethanol, isocaloric amounts of Lieber-DeCarli diet, or rat chow ad libitum for 6, 12, and 18 mo. In the ethanol-fed group, histologic studies by light microscopy showed absence of protein plugs in the pancreatic ducts and/or pancreatitis, but electron-microscopic evaluation revealed progressive accumulation of lipid droplets in acinar and ductal cells. No definite changes in the mitochondria and endoplasmic reticulum were noticed. Biochemical studies revealed increased specific activity of trypsinogen, chymotrypsinogen, and lipase, and decreased specific activity of amylase. Trypsin-inhibiting capacity was decreased in the tissue and in the medium in a progressive fashion. There was no increase in the secretion of total protein. These data show a complex and a nonparallel alteration of specific digestive enzymes and trypsin inhibitor in this model of chronic ethanol intoxication that may be of relevance to occurrence of pancreatitis.
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PMID:Pancreatic acinar cell function and morphology in rats chronically fed an ethanol diet. 617 13

The influence of hemorrhagic pancreatitis on pulmonary ultrastructure was investigated in 21 mongrel dogs. The animals were intubated but not ventilated. Pancreatitis was induced with an autologous bile-trypsin mixture. The degree of pancreatitis was confirmed clinically, chemically, and histologically. The animals were sacrificed at four time frames: zero time, one, three, and five hours after the onset of pancreatitis. There was progression, with time, of distorted pulmonary microarchitecture. Interstitial edema, including dispersion of endoplasmic reticulum, disruption of lamellar bodies, and blunting of the pseudopods in the type II pneumocyte, were noted. There was a decrease in osmiophilic content as well as loss of organization of the lamellar bodies. Since surfactant is produced and stored by the lamellar bodies in the type II pneumocyte, these data add support to the concept of pulmonary congestive atelectasis secondary to pancreatitis--related to absence of or diminished surfactant.
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PMID:Influence of hemorrhagic pancreatitis on the lung. An ultrastructural study. 660 24

Lactoferrin is a non-enzymatic secretory protein present in the acinar cells of human pancreas, and specifically increased in the pancreatic juice of chronic calcifying pancreatitis patients. Immunocytochemical localization of lactoferrin demonstrates its presence in the zymogen granules of the pancreatic acinar cell as well as in the endoplasmic reticulum cisternae. On the same section, only a few acini are positive but all cells within individual acini are similarly either positive or negative. The intensity of the reaction and the number of stained acini are greater in chronic calcifying pancreatitis patients.
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PMID:Immunocytochemical localization of lactoferrin in human pancreas. 734 87

By light and electron microscopic immunocytochemistry the distribution is described of human pancreatic elastase 1 (E1) during ontogenesis, in adults, in cases of acute and chronic pancreatitis, acute pancreatic ischaemia as well as pancreatic tumours. E1-positive cells were first detected in ductal sprouts in the 14th gestational week. Complete acini expressing E1 could be found from the 17th to the 20th week of gestation onwards. Scattered distinct E1-positive epithelia could be found in the ducts of fetal and adult pancreas. By immunoelectron microscopy, E1 was localized in rough endoplasmic reticulum, condensing vacuoles, zymogen granules of acinar epithelia and in acinar lumina. E1 appeared to be distributed homogeneously in zymogen granules. As specific markers of acinar cells, both monoclonal antibodies under study identified heterotopic pancreatic acini in peribiliar glands of the liver and also helped to visualize different damage patterns in pancreatitis. The acinar epithelia surrounding acute lipolytic necroses initially reacted more intensely with the E1-antibodies than undamaged pancreatic tissue. In acute ischaemia, acinar cells which are dissociated from intercalated ducts lost their immunocytochemical reactivity for E1. Pancreatic parenchyma involved in advanced acute pancreatitis as well as in chronic inflammation was detected only weakly by both E1-antibodies. However, atrophic lobules in post-inflammatory scars were stained more intensely by the E1-antibodies than normal parenchyma. Pancreatic tumours (adenomas, adenocarcinomas, solid-cystic tumours and islet cell tumours) were not labelled by these antibodies.
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PMID:Immunocytochemical localization of elastase 1 in human pancreas. 763 50

We studied in vivo and in vitro morphological aspects of pancreatic acinar cells after treatment with Tityus serrulatus venom (TSV). After three hours in an in vitro system, positive secretagogue effects of the venom were identifiable both at the light-microscopic (LM) and the electron-microscopic (EM) levels. At 1 microgram/ml TSV, maximal secretion (as measured in a concomitant radiolabeling dose-response experiment) of exocrine proteins at 58% was manifest as a discharge of most zymogen granules (ZG) and consequent appearance of secretory material in acinar lumina. At the supramaximal dose of 10 micrograms/ml TSV, exocytotic images were often observed also with secretory contents previously discharged. The lowest dose of venom at 0.01 microgram/ml caused no stimulation of zymogen discharge above resting secretion levels; however, morphological changes were observed. At high doses of TSV, both in vivo and in vitro, large aggregates associated with the cis-Golgi develop between this region and the endoplasmic reticulum (ER). Since Tityus venoms have been associated with causation of pancreatitis, we were interested in comparisons of our experimental tissue with parameters attributed to development of the disease. Our studies have demonstrated considerable evidence that large intracellular vacuoles, discharged ZG, effaced acinar lumina with disappearance of microvilli and other manifestations of possible early events in pancreatitis are indeed frequently observed both in pancreatic lobules in vitro and in whole pancreas in vivo when exposed to TSV.
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PMID:Morphological studies by light and electron microscopy of pancreatic acinar cells under the effect of Tityus serrulatus venom. 800 Oct 82


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