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Plasma Exudation (plasma + exudation)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Role of mast cells in the development of pancreatitis-induced multiple organ dysfunction

BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 2 2002
M. Dib
Background: Activated mast cells can produce and release a number of inflammatory mediators involved in the pathophysiology of acute conditions. The aim of the present study was to evaluate the role of activated tissue mast cells in the pathogenesis of multiple organ dysfunction syndrome following acute pancreatitis (AP). Methods: AP was induced by the intraductal infusion of 5 per cent sodium taurodeoxycholate in the rat. Some 30 min before induction of AP, a mast cell stabilizer (sodium cromoglycate (SCG)) or antihistamines (pyrilamine, cyproheptadine, meclizine and amitriptyline) were administered intra peritoneally. Plasma exudation of radiolabelled albumin, histamine, myeloperoxidase (MPO), monocyte chemoattractant protein (MCP) 1 and adhesion molecules (platelet endothelial cell adhesion molecule (PECAM) 1 and L-selectin) were measured. Results: The mast cell stabilizer significantly reduced plasma exudation in the pancreas, colon and lungs (P < 0·05), decreased the release of histamine at 1 h (P < 0·05), and reduced MPO activity and MCP-1 levels in the colon and lungs (P < 0·05) but not in the pancreas. Expression of PECAM-1 and L-selectin on total circulating leucocytes in rats with AP and SCG pretreatment did not differ from that in sham controls, while levels in animals that had AP and saline pretreatment were half of those seen following sham operation. Conclusion: Activation of mast cells after induction of AP is involved in the development of endothelial barrier dysfunction in both the pancreas and extrapancreatic organs/tissues, particularly in the lungs and colon. This may, at least partly, contribute to the sequential development of multiple organ dysfunction and organ/tissue-specific endothelial barrier dysfunction. © 2002 British Journal of Surgery Society Ltd [source]

Steroid-sensitive indices of airway inflammation in children with seasonal allergic rhinitis

PEDIATRIC ALLERGY AND IMMUNOLOGY, Issue 1 2003
Peter Meyer
Previous studies involving adults have demonstrated that airway glucocorticosteroids inhibit plasma exudation and eosinophil activity in allergic rhinitis. This study explores the possibility that plasma exudation, exudative responsiveness, and the occurrence of eosinophil activity-related proteins are glucocorticosteroid-sensitive nasal mucosal indices in allergic children. Using a placebo-controlled, parallel-group design effects of nasal budesonide (64 µg per nasal cavity b.i.d) were determined in children with seasonal allergic rhinitis. Nasal lavage fluid levels of eotaxin, eosinophil cationic protein (ECP), and ,2 -macroglobulin, indicating plasma exudation, were determined, the latter with and without challenge with topical histamine. Nasal lavage fluid levels of ,2 -macroglobulin and ECP increased significantly during the pollen season, and the acute plasma exudation response to histamine was significantly greater during than outside the season. There was a trend towards a seasonal increase in nasal lavage fluid levels of eotaxin. Budesonide significantly inhibited the seasonal increase in ,2 -macroglobulin as well as the exudative hyperresponsiveness to histamine. Any tendency of increases in mucosal output of eotaxin and ECP was abolished by the glucocorticosteroid treatment. We conclude that mucosal exudation of plasma, as a global sign of active inflammatory processes, is a glucocorticosteroid-sensitive facet of allergic rhinitis in children. Exudative hyperresponsiveness, potentially caused by several weeks of mucosal inflammation, emerges as a significant feature of allergic rhinitis in children, and its development is prevented by local treatment with a glucocorticosteroid drug. The seasonal increase in ECP and the trend for an increase in eotaxin were absent in the glucocorticosteroid-treated subjects. [source]

The effects of heparin and related molecules on vascular permeability and neutrophil accumulation in rabbit skin

BRITISH JOURNAL OF PHARMACOLOGY, Issue 2 2002
Helen Jones
Unfractionated heparin (UH) has been shown to possess a wide range of properties which are potentially anti-inflammatory. Many of these studies, including effects of heparin on adhesion of inflammatory cells to endothelium, have been carried out in vitro. In the present study, we have used radioisotopic techniques to study the effect of UH, and related molecules, on in vivo inflammatory responses (plasma exudation (PE) and PMN accumulation) in rabbit skin induced by cationic proteins, mediators and antigen. Intradermal (i.d.) pretreatment with UH dose-dependently inhibited poly-L-lysine (PLL)-induced responses. The same treatment had no effect on antigen (extract of Alternaria tenuis, AT)-, formyl-methionyl-leucyl-phenylalanine (fMLP)- or leukotriene (LT) B4 -induced responses, although i.d. dextran sulphate (DS) significantly inhibited responses to all of these mediators. High dose (10,000 u kg,1) intravenous UH significantly decreased cutaneous responses to fMLP and LTB4. By comparison, the selectin inhibitor, fucoidin, and DS, were very effective inhibitors of these responses, and of responses to AT and PLL. In contrast to the weak effect in the in vivo studies, UH significantly inhibited in vitro homotypic aggregation of rabbit PMNs, showing that it can modify PMN function. Our data with i.d. UH confirm the important ability of this molecule to interact with and neutralize polycationic peptides in vivo, suggesting that this is a prime role of endogenous heparin. The lack of effect of exogenous heparin on acute inflammatory responses induced by allergen, suggests that cationic proteins are unlikely to be primary mediators of the allergen-induced PE or PMN accumulation. British Journal of Pharmacology (2002) 135, 469,479; doi:10.1038/sj.bjp.0704505 [source]

Role of mast cells in the development of pancreatitis-induced multiple organ dysfunction

Cysteinyl leukotrienes as common mediators of asthma and allergic disease

CLINICAL & EXPERIMENTAL ALLERGY REVIEWS, Issue 2 2003
S-E. Dahlén
Summary The cysteinyl leukotrienes (CysLTs) induce a number of pro-inflammatory effects including smooth muscle contraction, an increase in blood flow, plasma exudation, mucous secretion, and activation of inflammatory cells. They play a key role in asthma and allergy, and can be recovered from different body fluids (e.g. bronchoaleveolar or nasal lavage and urine) during allergen-induced hypersensitivity reactions. The advent of antileukotriene agents (i.e. leukotriene receptor antagonists or leukotriene synthesis inhibitors) has helped clarify how the different mechanisms contribute to inflammation, as well as offer new treatment options for both asthma and allergy. It is now clear that the release of leukotrienes is the final common path for the many different factors causing airway obstruction and inflammation. In asthma, clinical studies have shown that treatment with antileukotrienes can improve pulmonary function, alleviate symptoms, reduce asthma exacerbations, and decrease the need for bronchodilator therapy. Similarly, in patients with allergic rhinitis, improvements have been seen in nasal symptoms, eye symptoms and quality of life. Antileukotrienes provide a new opportunity for simultaneous management of allergic diseases of the upper and lower respiratory tract, and are a rational treatment approach to the concept of ,one airway' disease. In future, their utility may also extend to inflammatory disorders of other organ systems (e.g. skin). [source]

Airway microvascular extravasation and luminal entry of plasma

CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 6 2003
Lennart Greiff
Summary Extravasation of plasma from postcapillary venules is a specific in vivo response to inflammatory insults. In the nasal and bronchial airways, extravasated plasma has a widespread distribution in the lamina propria, between the epithelial cells and in the airway lumen. This feature, in combination with the fact that the process involves extravasation of bulk plasma, with all peptides and proteins of plasma, indicates that plasma exudation contributes to the dramatic change of the mucosal milieu that characterizes airway inflammation. Accordingly, this process is of key importance to conditions such as allergic rhinitis and asthma. The means by which extravasated plasma participates in mucosal defence is physiological in the sense that it may operate on the surface of the epithelium without impairing its function as an absorption barrier. The flow of plasma into the airway lumen may thus wash away unwanted material from inter-epithelial cell spaces, exuded binding proteins may bind unwanted solutes non-specifically and extravasated immunoglobulins may neutralize allergens. In addition to the role as defence mechanism, extravasated plasma components may act as important pro-inflammatory factors. Furthermore, experimental data as well as observations in natural disease suggest that luminal levels of plasma proteins can be employed as an accessible index reflecting to what degree the airway mucosa is affected by inflammatory processes. [source]