Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031154 (peritonitis)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Soluble phospholipase A2 (PLA2) activity was assessed in rat peritoneal lavage fluid after an intraperitoneal injection of 6% glycogen. Enzyme activity immediately increased 5-fold above basal by 4 h. Activity decreased by only 30% at 18 h and remained at this elevated level through 72 h. The initial rise in PLA2 activity was coincident with protein extravasation but not with polymorphonuclear leukocyte infiltration, suggesting that the early PLA2 activity could be, in part, blood-derived. Mononuclear cell influx occurred later (4 h), peaked by 6-8 h but remained elevated through 72 h possibly contributing to the persistence of PLA2 activity through 20-72 h. The exudate PLA2 measured at 4-6 h (early) and 20-24 h (late), after glycogen administration, were biochemically compared. They were found to be neutral pH active, Ca(2+)-dependent and were similarly inhibited by the inhibitors, p-bromophenacylbromide, ellagic acid, gossypol and luffariellolide. Oral administration of dexamethasone to rats inhibited the appearance of PLA2 activity in the peritoneal lavage fluid as well as cellular influx and protein extravasation. Indomethacin had no effect on these parameters. These studies demonstrate that PLA2 is an integral component of glycogen-induced peritonitis and can be pharmacologically manipulated.
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PMID:Characterization and pharmacological modulation of soluble phospholipase A2 generated during glycogen-induced rat peritonitis. 145 81

In the experiment on 30 mongrel dogs, acute enzymatic cholecystitis (AEC) was modelled by means of intraduodenal connection with a fluoroplastic catheter of the common bile duct and pancreatic duct. The animals died at day 3-5 from transudative biliary peritonitis. A correlation between the severity of the clinical course, pronouncement of enzymologic shifts (increase in activity of amylase and phospholipase A2, content of biliary malonic dialdehyde) and morphological changes in the gallbladder and common bile duct in the form of necrosis and round-cell infiltration of the mucosa was revealed. Only decompression of the bile duct within the first 6 h from the moment of AEC development contributes to regression of clinical and enzymologic disorders and recovery of the animals.
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PMID:[Acute experimental enzymatic cholecystitis (clinico-morphological comparisons)]. 171 18

Intraperitoneal injection of zymosan into mice induces a peritonitis characterized by cellular influx, plasma leakage and the appearance of arachidonic acid (AA) metabolites. We report that zymosan injection also stimulates the accumulation of AA, docosahexaenoic acid, linoleic acid, and phospholipase A2 (PLA2) activity. The amount of the unsaturated fatty acids (UnFA) varies both with the zymosan dose and time. Significantly increased levels of UnFA were first detected 15 min after zymosan injection. Maximal levels of the UnFA were reached 1 to 2 h post zymosan injection (AA: 725 +/- 29 ng/mouse, docosahexaenoic acid: 296 +/- 23 ng/mouse, linoleic acid: 4489 +/- 179 ng/mouse) and declined to saline control levels by 8 h. PLA2 activity was significantly increased 5 to 15 min after zymosan injection. Maximal levels of PLA2 activity occurred 15 to 30 min after zymosan injection (31.8 +/- 9.1 nmol phospholipid/mg protein/h) and then decreased by 30% through 24 h. Neither the appearance of UnFA nor PLA2 activity correlated with cellular influx, but both were coincident with plasma exudation at 5 to 15 min after zymosan. However, maximal exudation occurred 1 to 2 h post zymosan injection similar to that seen with the UnFA but not PLA2. These latter results suggest that a significant portion of the UnFA found in the peritoneal cavity of zymosan-injected mice originates from the plasma. PLA2 activity at the early time points (5 to 15 min) may also contribute to the levels of UnFA via hydrolysis of tissue and/or cellular phospholipids.
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PMID:Kinetics of phospholipase A2, arachidonic acid, and eicosanoid appearance in mouse zymosan peritonitis. 210 9

The kinetics and appearance of extracellular phospholipase A2 (PLA2) activity and its relationship to the appearance of arachidonic acid (AA) metabolites in the peritoneal cavity of mice injected with zymosan is described. AA metabolites levels including leukotriene C4 (LTC4) were maximum 15-30 min after zymosan. Peak PLA2 activity was also found 15-30 min after zymosan and was significantly increased above levels found in saline control exudates (3.83 +/- 0.89 and 0.35 +/- 0.11, respectively, p less than or equal to 0.05). Results show that an extracellular PLA2 is present in zymosan peritonitis.
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PMID:Extracellular phospholipase A2 activity in cell free peritoneal lavage fluid from mice with zymosan peritonitis. 250 43

1. Using specific-pathogen-free New Zealand White rabbits, we have compared the effects of faecal peritonitis over a period of 5 h in eight test animals with eight controls in which a sham operation was performed. 2. There was morphological damage to lungs, liver and spleen of test animals. Lung capillaries and sinusoids of the liver showed occlusion by cell debris and leucocytes, with endothelial damage. The lungs also showed alveolar epithelial disruption, basement membrane exposure and type II pneumocytes lacking lamellar bodies. In the liver there was fibrin deposition and swollen Kupffer cells. The spleen showed degranulating neutrophils, fibrin deposits, platelet aggregates and activated macrophages, with no damage to the endothelium. 3. There was no morphological damage to the kidney or heart of test animals or to any organs of sham-operated animals. 4. There were mixed anaerobes and aerobes in faecal material used to induce peritonitis. Cultures of liver, spleen and kidney isolated four different types of micro-organisms. Blood cultures showed two types of micro-organisms. Cultures of lung and heart showed one type of micro-organism. 5. The presence of micro-organisms in an organ could not be correlated with the degree of histological damage to that organ. 6. In test animals an early significant reduction in circulating leucocytes and platelets was sustained for the duration of the experiment with significant diffuse intravascular coagulation. 7. There was no change in test animal neutrophil adhesiveness until 120 min, when significant reduction was observed. 8. Serum phospholipase A2 (EC 3.1.1.4) activity in the test group showed a threefold increase at 300 min.
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PMID:Multi-organ damage resulting from experimental faecal peritonitis. 252 65

To study the source and role of circulating phospholipase A2 (PLA2) catalytic activity we monitored the serum from patients with necrotizing pancreatitis (n = 8), diffuse peritonitis (n = 6), and multiple injuries (n = 11). Immunoreactive PLA2 serum protein concentration was analysed using a fluoroimmunoassay based on an antibody against human pancreatic PLA2. Serum PLA2 catalytic activity was analysed using a radiochemical method based on a substrate with tritiated palmitic acid in beta position. In necrotizing pancreatitis immunoreactive PLA2 and PLA2 catalytic activity both increased. Obviously, in necrotizing pancreatitis the major part of serum catalytic activity stems from the pancreas. In patients with diffuse peritonitis and multiple injuries, as a rule, immunoreactive phospholipase A2 serum concentration appears to be within the normal range. In contrast, in these patients we demonstrated high serum catalytic PLA2 activity comparable to that in necrotizing pancreatitis. The source of catalytic PLA2 activity in peritonitis and multiple injuries seems not to be the pancreas. There was a correlation between pulmonary insufficiency and serum PLA2 catalytic activity in patients with necrotizing pancreatitis, peritonitis, and multiple injuries.
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PMID:Serum phospholipase A2 in intensive care patients with peritonitis, multiple injury, and necrotizing pancreatitis. 292 58

The majority of intra-abdominal adhesions develop postoperatively or following peritonitis. We have previously shown that L-phosphatidylcholine reduces postoperative peritoneal adhesions in rats. In the present study, we examined whether adhesion formation after bacterial peritonitis is also reduced by L-phosphatidylcholine or by DL-alpha-phosphatidylcholine, which is degraded only 50% by phospholipase A2. Peritonitis was induced in the rat by caecal ligation and double puncture; cecotomy was performed 12, 15, or 18 h later. Adhesions were assessed blindly by a scoring system 7 days after cecotomy. When cecotomy was scheduled for 18 h after caecal ligation and puncture, the 7-day mortality was 90% (n = 20). When cecotomy was performed at 12 h, no mortality was seen; however, the adhesion score was low (2.3 +/- 0.7). When cecotomy was performed 15 h after caecal ligation and puncture, the mortality was 25% and the adhesion score was 4.3 +/- 0.9. This figure was reduced significantly by intraperitoneal instillation of L-phosphatidylcholine or DL-alpha-phosphatidylcholine for 3 subsequent days. However, the mortality increased by L-phosphatidylcholine (P < 0.01), whereas mortality after DL-alpha-phosphatidylcholine remained at 30%. We conclude that administration of both L-phosphatidylcholine and DL-alpha-phosphatidylcholine decrease adhesion formation after bacterial peritonitis.
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PMID:Phospholipase-resistant phosphatidylcholine reduces intra-abdominal adhesions induced by bacterial peritonitis. 851 62

Multiple organ failure (MOF) is the most common cause of death in the surgical intensive care unit. We studied the relation of MOF to changes in the concentration of group II phospholipase A2 (PLA2) in serum. Altogether, 215 surgical intensive care patients with multiple injuries, diffuse peritonitis, or sepsis and control patients, who were at a high risk for postoperative sepsis after various surgical interventions, were included in the present prospective study. The clinical performance of the MOF score and the concentrations of group II PLA2 and C-reactive protein (CRP) in serum were studied using receiver operating characteristic (ROC) curves. The group II PLA2 level was considerably above normal in all groups of patients during the first week of observation. There was a highly significant difference in group II PLA2 levels between patients with severe infections (peritonitis and sepsis) and the other patients studied (multiple injuries and elective surgery) (ROC 0.931, P < 0.0001). The concentration of group II PLA2 had a significant positive correlation to the CRP level and body temperature, which indicates that group II PLA2 is an acute phase reactant and that the determination of group II PLA2 is a useful measurement to diagnose severe infections. It was concluded that the concentration of group II PLA2 in serum effectively predicts lethal MOF in patients with multiple injuries after the second day (ROC 0.739, P < 0.01) and in patients with diffuse peritonitis after the fourth day (ROC 0.750, P < 0.02).
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PMID:Serum phospholipase A2 in patients with multiple organ failure. 859 35

The plant Crataegus monogyna has action against cardiac insufficiency, angina and arrhythmia. The anti-inflammatory properties of the cycloartenol fraction from this plant have been investigated. Chromatographic fractionation of the hexane extract of Crataegus monogyna Jacq. (Rosaceae) furnished a triterpene fraction containing cycloartenol as the main component (80.87%). The anti-inflammatory activity of the fraction was tested against hind-paw oedema induced by carrageenan in rats. At the highest oral dose (40 mg kg-1) inhibition was 61.5 and 52.5% at 3 and 5 h respectively. In the mouse carrageenan peritonitis test, the triterpene fraction given orally inhibited peritoneal leucocyte infiltration (41.9, 64.7 and 89.4% at 10, 20 and 40 mg kg-1, respectively). The fraction also showed weak inhibition of phospholipase A2 (PLA2) in-vitro. These results suggest that the fraction containing cycloartenol as the main component exerts an important anti-inflammatory action in-vivo by reducing the oedema.
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PMID:The effects of a triterpene fraction isolated from Crataegus monogyna Jacq. on different acute inflammation models in rats and mice. Leucocyte migration and phospholipase A2 inhibition. 923 56

The alterations in peritoneal permeability characteristics during peritonitis can only partly be explained by the increased concentrations of prostaglandins and cytokines in the dialysate. Fifteen patients undergoing continuous ambulatory peritoneal dialysis (CAPD) with 16 peritonitis episodes were examined in the acute phase of the infection by using standard peritoneal permeability analyses (SPAs). In 9 of these patients, a control SPA could be performed. The contribution of nitric oxide (NO), prostaglandins, and the acute phase reactants C-reactive protein (CRP) and secretory phospholipase A2 (sPLA2) were analyzed. The mass transfer area coefficients (MTACs) of low-molecular-weight solutes increased during peritonitis: urea 26%, creatinine 45%, and urate 45%. The MTAC of CO2, calculated to estimate peritoneal blood flow, was 71 mL/min (34 to 254 mL/min) during peritonitis and 55 mL/min (42 to 63 mL/min) after recovery, P < or = .05. The peritoneal protein clearances were also greater during peritonitis, but this increase was not related to the molecular weight of the protein. Therefore the restriction coefficients to macromolecules were not different. The net ultrafiltration in all peritonitis episodes was lower as compared with the control dwells: -97 mL (-196 to 19 mL) versus 25 mL (-132 to 216 mL), P = .03. The prostaglandin concentrations in dialysate were greater during peritonitis than after recovery. The median increase was 199% for prostaglandin E2 (PGE2), 68% for 6-keto-prostaglandin F1alpha (6-keto-PGF1alpha), and 44% for thromboxane B2 (TxB2). Plasma sPLA2 values were 22.7 microg/L (7.3 to 407.6) during peritonitis and 8.9 microg/L (5.5 to 11.5) after recovery, P < .01. The increased plasma sPLA2 during peritonitis correlated with plasma CRP (r = .6; P = .02). The peritoneal clearances of sPLA2 were greater during peritonitis, but this could be attributed completely to the increased peritoneal transport. Both during peritonitis and after recovery, the sPLA2 clearances did not exceed the predicted values based on transport from the circulation to the dialysate. No evidence was found for local production of nitrite or nitrate. However, the MTAC of cyclic guanosine monophosphate (cGMP) was greater during the experiments performed 48 to 72 hours after the onset of peritonitis, which suggests the synthesis of NO. It can be concluded that peritonitis does not induce detectable local release of sPLA2 and that the inflammation-induced increase in the vascular surface area could not be attributed to NO in the acute phase. The activation of inducible NO synthase may occur after 48 hours.
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PMID:Are phospholipase A2 and nitric oxide involved in the alterations in peritoneal transport during CAPD peritonitis? 979 5


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