Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human urinary kallikrein and an antiserum to it raised in the rabbit were used to detect and quantitate immunoreactive tissue kallikrein in human serum. Both 125I-labeled kallikrein and the unlabeled purified enzyme appear complexed to higher molecular weight entities in serum, but specific binding between radiolabeled enzyme and antiserum was unaffected by the presence of serum or plasma. Parallelism to standard displacement curves was always seen with radioimmunoassay of normal sera as well as with human mixed saliva or pancreatic extracts. Assay sensitivity is 160 pg/ml of serum, or 16 pg per tube. Purified plasma kallikrein or prekallikrein in concentrations up to 10 micrograms/ml showed no displacement. Acetone-kaolin activation of plasma produced the expected 30-fold increase in Tos-Arg-OMe esterase activity but no change in immunoreactive tissue kallikrein levels. Serum concentrations were 3.8 +/- 0.7 (mean +/- SE) ng/ml in 21 normal volunteers, and were similar in patients with Fletcher trait or Hageman factor deficiency. Significantly increased serum concentrations were seen with long-term low dietary sodium intake or acute forms of pancreatitis. Although the relation of this immunoreactive material to any active tissue kallikrein within the circulation remains to be determined, our studies provide a new parameter for the assessment of a system repeatedly suggested to have some role in regulation of vascular resistance.
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PMID:Immunoreactive tissue kallikrein in human serum. 656 56

The endocrine secretory function of rat pancreases in which pancreatitis had been induced by feeding rats a 0.5% ethionine diet was investigated. Despite loss of 50% of exocrine tissue and widespread destruction of acinar structure, pancreatic insulin and glucagon contents and 4-h fasting plasma insulin levels in vivo did not differ significantly from those of food-restricted, weight-matched controls. Plasma glucose concentrations (fasting and after oral glucose) were significantly lower than control. In isolated, perfused ethionine-treated pancreases secretin failed to stimulate insulin secretion, whereas basal insulin secretion and insulin responses to glucose, arginine, gastric inhibitory polypeptide, vasoactive intestinal peptide (VIP), and somatostatin were similar to those of controls. Basal glucagon secretion was elevated in ethionine-treated pancreases, and glucagon outputs in response to arginine, VIP, and somatostatin showed a consistent trend toward higher levels than those of controls. These findings demonstrate that ethionine-induced pancreatitis selectively impairs islet secretory function. These effects may be due to damage to islet cell membranes by exocrine enzymes and/or a direct pathogenic action of ethionine on the islets.
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PMID:Altered insulin and glucagon secretion in perfused ethionine-treated rat pancreases. 675 65

Previous reports regarding the effect of an elemental diet (ED) on pancreatic secretion have been conflicting. This study was designed to assess the effect of a high-nitrogen ED or total parenteral nutrition (TPN) on proteolytic activity in the pancreatic exocrine cell. Forty-eight dogs were divided into 12 groups of 4 each. Group I (control) was fed commercial dog food. Groups II, III, and IV received 1, 2, and 3 days, respectively, of 25% glucose with 4.25% amino acids. Groups V, VI, and VII received 1, 2, and 3 days, respectively, of 25% glucose with 2.75% amino acids. Groups VIII, IX, and X received 3 days of ED given orally, via gastrostomy or jejunostomy, respectively. Groups XI and XII received 1 day each of either 2.75% amino acids or 25% glucose. The pancreas of each dog was then resected and processed for electron microscopy, or minced and analyzed for tryptic activity expressed as micromoles of benzoyl arginine ethyl ester (BAEE) digested per milligram of pancreatic protein. There were no significant differences in ultrastructure or in the levels of pancreatic tryptic activity between the control and the 11 experimental groups. It appears that during the short period of our treatment with TPN as well as ED, the exocrine cell retains its normal content of proteolytic enzyme. Reports of others that pancreatic secretion volume decreases with TPN and ED, coupled with our findings of stable intracellular tryptic activity, indicate that the synthesis and release of proteolytic enzymes have actually been reduced by TPN and ED. Thus, TPN or ED should benefit the patient with pancreatitis by decreasing pancreatic secretion as well as pancreatic proteolytic enzyme synthesis.
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PMID:The effect of total parenteral nutrition or elemental diet on pancreatic proteolytic activity and ultrastructure. 680 Dec 82

Evidence is present that plasma contains non-specific factors which interfere with the 30K glucagon assays. A correction can be made for these interference factors because the factors can be quantitated following absorption of glucagon with charcoal-dextran. Using a correction factor the range of fasting plasma immunoreactive glucagon (IRG) in 12 totally pancreatectomized patients was below detectable limit. Fasting levels of IRG were determined on the plasma from 25 liver cirrhotics complicated by abnormal GTT, 13 pancreatic diabetics with chronic calcified pancreatitis (CCP), 25 adult-onset primary diabetics and 25 healthy subjects. When all samples were measured using no correction factor, the mean levels of IRG were 358 +/- 24 (mean +/- SE), 170 +/- 26, 178 +/- 16 and 178 +/- 7 pg/ml, respectively. Using a correction factor the mean level of IRG were 177 +/- 26, 16 +/- 4, 39 +/- 9 and 20 +/- 4 pg/ml, respectively. The mean values of the interference factor were not significantly different among all five groups. During an arginine infusion the interference factor remained unchanged despite an increase in IRG. It is available but not always necessary to apply a correction factor for 30K glucagon radioimmunoassay.
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PMID:Plasma pancreatic glucagon in pancreatic and primary diabetes, and liver cirrhosis: application of a correction to the radioimmunoassay for pancreatic glucagon. 714 Nov 99

Levels of free amino acids were analysed in plasma and muscle tissue of nine patients with acute hemorrhagic necrotising pancreatitis and compared with date from healthy volunteers. In the patient group the concentrations of threonine, serine, glutamine (p less than 0.001) and tyrosine (p less than 0.01) in plasma were found to be significantly lower than in the volunteers group, while increased plasma levels were found for 3-met-histidine (p less than 0.05). In muscle tissue the cytoplasmatic levels of glutamate, glutamine and histidine (p less than 0.001) and also of lysine, ornithine and arginine (p less than 0.,01) showed decreased concentrations. However tyrosine and phenylalanine had increased intracellular concentrations (p less than 0.05). It is concluded that (1) the patients in this study had a severely disturbed amino acid metabolism with extremely reduced levels of free glutamine in muscle tissue and (2) that the disturbed amino acid metabolism results from an acute catabolic situation of the patients, in which the reduced levels of free amino acids may indicate an impaired nutritional state.
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PMID:[Reduced levels of free amino acids in plasma and muscle tissue of patients with acute hemorrhagic necrotising pancreatitis (author's transl)]. 723 25

The aim of the present study was to determine the role of endogenous nitric oxide (NO) in pancreatic secretion in vivo and amylase release from pancreatic acini in vitro and in caerulein-induced acute pancreatitis in rats. Blockade of NO synthase by NG-nitro-L-arginine (L-NNA) (2.5 mg/kg i.v.) significantly reduced basal pancreatic protein secretion and that induced by the infusion of CCK (0.5 micrograms/kg-h), feeding, and the diversion of pancreatic juice in rats with pancreatic fistula. This inhibitory effect was partially reversed when L-arginine (50 mg/kg-h i.v.) was added to L-NNA. L-Arginine alone (50 mg/kg i.v.) did not affect basal or caerulein-induced pancreatic secretion. L-NNA, L-arginine, or their combination added in various concentrations to the incubation medium of dispersed acini failed to affect basal or secretagogue (caerulein or urecholine) stimulated amylase release. Infusion of caerulein (5 micrograms/kg-h) for 5 h produced histological changes of acute edematous pancreatitis accompanied by a marked increase in pancreatic protein content and about 50% reduction in tissue blood flow. L-NNA alone also reduced the pancreatic blood flow and caused a significant increase in pancreatic weight and protein content. L-NNA significantly potentiated the inflammatory changes in the pancreas caused by caerulein. Addition of L-arginine enhanced the pancreatic blood flow and ameliorated the pancreatitis induced by caerulein alone or that combined with L-NNA. We conclude that NO is involved in the stimulation of pancreatic secretion in vivo and exhibits a beneficial effect on pancreatitis, probably by improving the pancreatic blood flow.
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PMID:Nitric oxide in pancreatic secretion and hormone-induced pancreatitis in rats. 751 91

Nitric oxide (NO) has been implicated to regulate pancreatic circulation, promote capillary integrity, and inhibit leukocyte adhesion. We investigated the role of NO in the development of pancreatitis. Nitro-L-arginine, an inhibitor of NO synthase, in total dose of 35 mg/kg body wt was infused in the rats with edematous pancreatitis induced by two intraperitoneal injections of cerulein (20 micrograms/kg). L-Arginine (125 or 250 mg/kg), a NO donor was intravenously administered twice in the rats with hemorrhagic pancreatitis induced by water-immersion stress plus two intraperitoneal injections of cerulein (40 micrograms/kg). The degree of pancreas edema, serum amylase levels, and histologic alterations were investigated. Nitro-L-arginine exacerbated cerulein-induced pancreatitis and caused a decrease in pancreatic blood flow. L-Arginine ameliorated the severity of hemorrhagic pancreatitis dose dependently and improved the pancreatic blood flow. These findings suggest that NO could confer protection against the development of hemorrhagic pancreatitis, probably through improvement of the pancreatic microcirculation.
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PMID:Protective effect of nitric oxide on development of acute pancreatitis in rats. 758 83

This study evaluated the effect of varying the synthesis of nitric oxide with sodium nitroprusside or N-nitro-L-arginine methyl ester (L-NAME) in a pancreatitis-lung injury model. Rats (n = 45) were randomized to control or caerulein-induced pancreatitis groups, treated with saline, sodium nitroprusside (0.4 micrograms/kg) or L-NAME (10 mg/kg). Myeloperoxidase activity was used as a measure of neutrophil infiltration. Wet to dry (W:D) lung weight and bronchoalveolar lavage (BAL) protein concentrations were used to assess vascular leakage. Pancreatitis was shown to induce pulmonary neutrophil influx: mean(s.e.m.) myeloperoxidase activity 6.79(0.5) units/g in caerulein-treated animals versus 2.08(0.5) units/g in controls (P < 0.001). Animals with pancreatitis showed increased microvascular leakage compared with controls (mean(s.e.m.) W:D lung weight 7.01(0.5) versus 2.85(0.2), P < 0.001; BAL protein concentration 2539(222) versus 347(32) micrograms/ml, P < 0.001). Compared with the saline-treated pancreatitis group, these changes were reduced by sodium nitroprusside (mean(s.e.m.) myeloperoxidase activity to 2.5(0.4) units/g, P < 0.001; W:D lung weight to 3.8(0.37), P < 0.001; BAL protein concentration 1389(182) micrograms/ml, P < 0.05). L-NAME exacerbated the pancreatitis-induced pulmonary oedema (W:D lung weight increased to 11.96(0.6), P < 0.001), protein leakage (BAL protein concentration rose to 3707(309) micrograms/ml, P < 0.05) and neutrophil infiltration (myeloperoxidase activity increased to 9.01(0.3) units/g, P < 0.05). These data suggest that, in vivo, nitric oxide inhibits pancreatitis-induced lung injury, possibly in part by inhibiting pulmonary neutrophil influx.
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PMID:Role of nitric oxide in lung injury associated with experimental acute pancreatitis. 764 71

The effect of bradykinin on nitric oxide generation and eicosanoid production in the early stage of an experimental model of acute necrotizing pancreatitis induced by sodium taurocholate has been evaluated. We have compared the effect of administering a long-acting bradykinin antagonist, HOE 140, and an inhibitor of nitric oxide synthase, NG-nitro-L-arginine methyl esther L-NAME) on pancreatic prostanoid synthesis. Plasma lipase levels were increased after acute pancreatitis induction, and reduced after HOE 140 or L-NAME administration. Nitric oxide production and thromboxane B2 levels were increased after pancreatitis induction and the increases were reduced by L-NAME or HOE 140 administration. In contrast, increased prostacyclin production, reflected as 6-keto-PGF1 alpha levels, was not modified by L-NAME or HOE 140. Bradykinin seems to be involved in nitric oxide and thromboxane synthesis during the initial phases of acute necrohemorrhagic pancreatitis.
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PMID:A bradykinin antagonist inhibited nitric oxide generation and thromboxane biosynthesis in acute pancreatitis. 765 83

The role of nitric oxide in eicosanoid and oxygen-free radical production in the early stages of sodium taurocholate-induced acute necrotizing pancreatitis has been studied. Male Wistar rats were divided into three groups: group I: control group, a volume of 0.1 ml/100 g body wt saline solution was injected at low pressure in the pancreatic duct; group II: acute pancreatitis was induced by administration of 3.5% sodium taurocholate; and group III: intravenous administration of NG-nitro-L-arginine methyl esther (a nitric oxide synthase inhibitor) 5 min before induction of acute pancreatitis as stated for group II. At 5 and 60 min after induction of pancreatitis, blood and pancreas tissue samples were taken for assays. Increases in 6-keto PGF1 alpha, TXB2, PGE2, PGF2 alpha, and 12-HETE were observed in the pancreatic tissue. Lipoperoxidation was also enhanced and remained unaltered after nitric oxide inhibition. The fact that nitric oxide synthase inhibition could only reverse the increases in 6-keto PGF1 alpha and TXB2 levels indicates that in acute pancreatitis endothelial and platelet eicosanoid generation is mediated through an nitric oxide-dependent mechanism. In contrast, nitric oxide appears to be not related with oxygen free radical damage associated with acute pancreatitis.
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PMID:Prostanoid generation in early stages of acute pancreatitis: a role for nitric oxide. 784 92


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