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

The inflammatory process in pancreas affects the function and structure of kidneys both by enzymatic toxemia and impairment of the renal circulation. In this study the stability of renal lysosomes in AEP in dogs treated with cytoprotective agent PGI2 was investigated. AEP was induced by injection of the bile and trypsin into the pancreatic duct; experiments were terminated after 12 hours. In lysosomal enriched subfraction of the kidney cortex (sedimenting in 15 000 x g) in untreated group (N = 5) relative free activity (r.f.a.) of cathepsins (Cs), acid phosphatase (APh) and beta-glucuronidase (BG) increased to 51,67 and 62% respectively, whereas in healthy dogs (N = 6) these activities were 20,38 and 25%. In dogs (N = 6) treated with PGI2 at the dose of 20 ng/kg/min. during 12 hrs, the r.f.a. of Cs, APh and BG was 18,40 and 49%, whereas in dogs (N = 5) additionally pretreated during 1 hr before induction of AEP with the same dose of PGI2, its values achieved 19,40 and 47% respectively. Our results suggest the stabilizing effect of PGI2 on kidney lysosomes damaged in acute experimental pancreatitis in dog. As possible mechanisms of prostacyclin action are discussed: limitation of necrotic process in the pancreas; improvement of renal haemodynamics; direct cytoprotective effect on the kidney.
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PMID:The renal lysosomes in acute experimental pancreatitis in dogs treated with prostacyclin (PGI2). 637 45

Majority of literature data support the significance of proteases activation in pathogenesis of acute pancreatitis. The ability of cathepsins to the activation of trypsinogen was shown and the labilization of lysosomes of pancreas in different models of acute experimental pancreatitis (AEP) was reported. In present work the dynamic of lysosomal changes during the course of AEP in dogs is evaluated. AEP was induced in 17 mongrel dogs by Elliot's method. Six healthy dogs served as a control group (I). Pancreatitic dogs were killed after 6 hr (G. II, n = 5), after 12 hrs (G. III, n = 5), and after 24 hrs (G. IV, n = 6 survivors). The pancreata were removed and divided into segments A (less advanced changes, [B] most advanced changes) and C (intermediate changes). The lysosomal enriched subfraction was isolated from the C segments at 15 000 X g for 20 min. The total (T) and free (F) activity of beta-glucuronidase (beta-G), acid phosphatase (AP), acid cathepsins (Cs) was estimated and the value F/T (relative free activity-r.f.a.) was calculated as an index of lysosomal stability. The progressive increase of r.f.a. of hydrolases in whole homogenate and in lysosomal enriched subfraction depending on time of AEP was observed suggesting labilization of pancreatic lysosomes. This labilization was more expressed in corresponding parts of organ with more advanced pathological changes. The differences between part A and B were most evident after 6 hrs of AEP. The labilization of lysosomes is more pronounced after 12 and 24 hrs than after 6 hrs in analogical parts of organ. These results indicate that labilization of lysosomes in pancreas correspond to the degree of pathological changes of pancreatic tissue.
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PMID:Pancreatic lysosomal hydrolases in acute experimental pancreatitis in dogs. 651 6

Rats infused with a supramaximally stimulating dose of the cholecystokinin-pancreozymin analogue caerulein develop acute interstitial pancreatitis (M. Lampel and H.F. Kern. Virchows Arch. A 373: 97-117, 1977). We have studied the early (30-180 min) morphological changes in pancreatic acinar cells induced by infusing caerulein (2.5 micrograms X kg-1 X h-1). The techniques of thin-section electron microscopy, freeze fracture, and enzyme and immunocytochemistry were employed. Shortly (30 min) after the onset of caerulein infusion, large vacuoles appeared in the Golgi area. After longer periods of infusion, these vacuoles further enlarged (probably by fusion with other such vacuoles as well as autophagic vacuoles) and became more widely distributed in the cytoplasm. These large vacuoles were found to be acid phosphatase positive and to be labeled by antibodies directed against digestive zymogens as well as the lysosomal enzyme cathepsin D. These observations indicate that the large vacuoles contain both digestive zymogens and lysosomal hydrolases. During caerulein infusion, morphological evidence of exocytosis at the luminal plasmalemma was reduced or absent, and evidence of basolateral exocytosis was not noted. These studies suggest that secretagogue hyperstimulation with caerulein interferes with the processes involved in condensing vacuole maturation, which normally lead to the separation of digestive zymogens and lysosomal hydrolases. As a result, both types of enzymes remain within the same compartment. This may lead to the intracellular activation of digestive enzymes by lysosomal hydrolases and be an important step in the development of acute pancreatitis.
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PMID:Supramaximal caerulein stimulation and ultrastructure of rat pancreatic acinar cell: early morphological changes during development of experimental pancreatitis. 672 Aug 95

In 15 mongrel dogs acute experimental pancreatitis (AEP) was induced by injection of bile and trypsin into the pancreatic duct. After 12 hrs in lysosomal enriched subfraction of the liver in untreated group (N = 5) relative free activity of cathepsins (Cs), acid phosphatase (AP) and beta-glucuronidase (beta G) increased to 50,62, and 53% respectively in comparison to the healthy dogs (N = 6) : 19,43 and 20%. In dogs with AEP treated with prostacyclin (PGI2) in the dose of 20 ng/kg X min for 12 hrs these activities of Cs, AP and beta G were lowered to 30,55 and 41% in comparison with the untreated group. In dogs with AEP (N = 5) additionally pretreated during 1 hr before the induction of AEP with the same rate of PGI2 i.v. infusion, the relative free activity of enzymes was similar to the treated group. After two hrs incubation of lysosomal enriched subfraction in acidic medium (pH = 5,0), the highest values of relative free activity were observed in untreated group, the difference being more pronounced in comparison with control group than before incubation. In those animals treated and pretreated with PGI2, postincubation activities were much lower than in untreated dogs. These results suggest the stabilising effect of PGI2 on hepatic lysosomes, damaged during the course of AEP in dogs.
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PMID:Prostacyclin (PGI2) stabilises hepatic lysosomes during acute experimental pancreatitis in dogs. 675 74

Nine lysosomal enzymes and alkaline phosphatase have been assayed in human pancreatic juice from controls and patients with chronic calcifying pancreatitis. Specific activities were evaluated by a nonparametric test (Wilcoxon) with a probability of 2 P less than or equal to 0.5. The values of acid phosphatase, alpha-glucosidase, beta-glucosidase and alpha-galactosidase are significantly higher in pathological juices; the values of alpha-mannosidase and beta-glucuronidase are also increased in the same patients but at the limit of significance. Alkaline phosphatase, beta-hexosaminidase and alpha-fucosidase follows the same trend but the values are not statistically significant between the two groups of patients. Studies on skin cultures of four patients with chronic calcifying pancreatitis demonstrate that the increased specific activities of lysosomal enzymes in the pathological juices do not correspond to a leakage of these enzymes into the extracellular space as described for cystic fibrosis.
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PMID:Alkaline phosphatase and acid lysosomal hydrolases in pancreatic juice and fibroblast cell cultures of patients with chronic calcifying pancreatitis. 680 85

Experiments on rats have demonstrated that changes in the serotonin level in the body intensifies pancreatic function. The pancreas shows the increased contents of trypsinogen and proelastase and those of lysosomal enzymes (cathepsins and acid phosphatase). Administration of serotonin leads to the reduction of the inhibitory properties of blood serum versus proteolytic pancreatic enzymes. Administration of serotonin to animals with the preliminarily ligated pancreatic duct results in the development of pancreatitis with a pronounced fat necrosis of the pancreatic tissue.
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PMID:[Effect of serotonin on secretory and lysosomal enzyme activity in pancreatic tissue and the inhibitory properties of serum]. 691 1

We have previously demonstrated a direct relationship between the activity of the arachidonic acid cascade in vivo and the extent of cellular damage following several types of experimental injury. Since phospholipase activity has been shown to regulate arachidonic acid availability, we tested the ability of circulating phospholipase A2 (PLA2) of pancreatic origin to stimulate prostanoid production or induce cellular injury in the isolated, perfused rabbit liver. Experimental conditions were similar to those present during pancreatitis or early splanchnic artery occlusion shock. The administration of PLA2 at a rate of 100 U/min for 10 min resulted in enhanced rates of thromboxane B2 and 6-ketoprostaglandin F1 alpha release between 1 and 5 min into the infusion period. No changes in hepatic perfusion pressure, vascular resistance, wet tissue weight, or release of lactic dehydrogenase or acid phosphatase into the effluent were observed in either vehicle or PLA2-treated livers. This indicates that cellular injury was not a factor in the prostanoid release. These data suggest that circulating PLA2 can directly stimulate de novo prostanoid synthesis in noninjured tissues. Thus, enhanced plasma prostanoid concentrations in intact animals during periods or regional cellular injury may be due in part to circulating PLA2 released from damaged tissues.
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PMID:Phospholipase A2 stimulated release of prostanoids from the isolated, perfused rabbit liver: implications in regional cellular injury. 733 80

The role of lysosomal hydrolases in the pathogenesis of acute pancreatitis and secondary liver injury, as an important aspect of multisystem organ failure, remains unclear. The purpose of this study was to assess the lysosomal fragility in both organs in acute experimental pancreatitis (AEP) of graded severity in dogs. In 7 dogs, the moderate (M) and in 13 dogs severe (S) variant of bile--trypsin AEP--was induced; 6 dogs were in control group (C). The 24 h survival time was 6/7 and 6/13, respectively. After that time, the dogs were sacrificed and the lysosomal enriched subfraction (L) from both organs was isolated by ultracentrifugation. The total (T) and free (F) activities of beta-glucuronidase (beta G), cathepsins (Cs) and acid phosphatase (AcP) according to Gianetto and de Duve were assayed. The fractional free activity (% F/T) was adapted as and index of lysosomal stability. The %F/T of BG in the homogenate of the pancreas in AEP(S) was higher than that in AEP(M) (92% vs. 71%, p < 0.05, and vs. 37% in C, p < 0.005). The %F/T of Cs and AcP showed a similar pattern. The %F/T of beta G in L of the liver in AEP(S) was 38% vs. 29% in AEP(M), (p < 0.05), and vs. 20% in C (p < 0.05). In AEP in dogs the %F/T activities of lysosomal hydrolases in the pancreas and liver were increased, suggesting the labilization of lysosomal membranes in severe form of this disease. Our results support the pathogenic role of lysosomal hydrolases in the damage to the pancreas and liver in acute pancreatitis.
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PMID:The role of lysosomal alterations in the damage to the pancreas and liver in acute experimental pancreatitis in dogs. 752 Sep 59

The main purpose of this study was to investigate the influence of early total parenteral nutrition on acute sodium-taurocholate-induced pancreatitis in rats. Total parenteral nutrition did not change the survival rate, serum amylase, calcium or liver transaminase level on the degree of pancreatic damage, but reduced serum acid phosphatase and lactate dehydrogenase levels. Hyperglycemia occurred during the use of total parenteral nutrition. Total parenteral nutrition is not harmful in the course of acute experimental pancreatitis, and could be used with few side effects.
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PMID:The influence of early total parenteral nutrition on experimental pancreatitis in rats. 768 45

The decompartmentation of lysosomal compartment in pancreatic acinar cells with consecutive activation of zymogens might play an important role as a "trigger mechanism" in acute pancreatitis. The admixture of lysosomal hydrolases to secretory enzymes in pancreatic juice was found, but their role in pancreatic secretion remains obscure. The aim of the present study was to assess the fragility of pancreatic lysosomal structure after maximal (optimal) or supramaximal stimulation of rats with cerulein during 3, 6, 12 h, and after recovery. In the mitochondrial-lysosomal (M-L) and in the supernatant (S) of pancreases free (F) total (T), and fractional free (%F/T) activities of beta-glucuronidase (beta G), acid phosphatase (AcP), cathepsins (Cs), and beta-N-acetyl-hexosaminidase (NAH) were estimated. In edematous pancreatitis following supramaximal stimulation with cerulein, a significant increase of %F/T of beta G in whole homogenate began at 6 h of hyperstimulation in comparison to the control (93 vs 42% p < 0.01). This increment persisted until 12 h of hyperstimulation and declined after 24 and 48 h of recovery to 67-69%. The changes of %F/T of beta G in M-L followed those in whole homogenate, and additionally the increase free activity in S after 6 h of hyperstimulation and after 24 h recovery occurred. The respective activities of other hydrolases showed a similar pattern of changes. It is of interest that fragility of lysosomal membranes increases significantly also after maximal stimulation when inflammatory changes were absent. Our results suggest that the increase of lysosomal fragility of the pancreas is most unlikely pathological in itself, but also occurs during stimulated pancreatic secretion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The lysosomal hydrolases in the rat pancreas after maximal or supramaximal stimulation with cerulein. 780 14


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