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Plasma Leakage (plasma + leakage)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Vascular endothelium: the battlefield of dengue viruses

FEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 3 2008
Atanu Basu
Abstract Increased vascular permeability without morphological damage to the capillary endothelium is the cardinal feature of dengue haemorrhagic fever (DHF)/dengue shock syndrome (DSS). Extensive plasma leakage in various tissue spaces and serous cavities of the body, including the pleural, pericardial and peritoneal cavities in patients with DHF, may result in profound shock. Among various mechanisms that have been considered include immune complex disease, T-cell-mediated, antibodies cross-reacting with vascular endothelium, enhancing antibodies, complement and its products, various soluble mediators including cytokines, selection of virulent strains and virus virulence, but the most favoured are enhancing antibodies and memory T cells in a secondary infection resulting in cytokine tsunami. Whatever the mechanism, it ultimately targets vascular endothelium (making it a battlefield) leading to severe dengue disease. Extensive recent work has been done in vitro on endothelial cell monolayer models to understand the pathophysiology of vascular endothelium during dengue virus (DV) infection that may be translated to help understand the pathogenesis of DHF/DSS. The present review provides a broad overview of the effects of DV infection and the associated host responses contributing towards alterations in vascular endothelial cell physiology and damage that may be responsible for the DHF/DSS. [source]

Cytokine cascade in dengue hemorrhagic fever: implications for pathogenesis

FEMS IMMUNOLOGY & MEDICAL MICROBIOLOGY, Issue 3 2000
U.C. Chaturvedi
Abstract Dengue virus produces a mild acute febrile illness, dengue fever (DF) and a severe illness, dengue hemorrhagic fever (DHF). The characteristic feature of DHF is increased capillary permeability leading to extensive plasma leakage in serous cavities resulting in shock. The pathogenesis of DHF is not fully understood. This paper presents a cascade of cytokines, that in our view, may lead to DHF. The main feature is the early generation of a unique cytokine, human cytotoxic factor (hCF) that initiates a series of events leading to a shift from Th1-type response in mild illness to a Th2-type response resulting in severe DHF. The shift from Th1 to Th2 is regulated by the relative levels of interferon-gamma and interleukin (IL)-10 and between IL-12 and transforming growth factor-,, which showed an inverse relationship in patients with DF. [source]

Development of Silicone Rubber Hollow Fiber Membrane Oxygenator for ECMO

ARTIFICIAL ORGANS, Issue 11 2003
Tadashi Motomura
Abstract:, Silicone rubber hollow fiber membrane produces an ideal gas exchange for long-term ECMO due to nonporous characteristics. The extracapillary type silicone rubber ECMO oxygenator having an ultrathin hollow fiber membrane was developed for pediatric application. The test modules were compared to conventional silicone coil-type ECMO modules. In vitro experiments demonstrated a higher O2 and CO2 transfer rate, lower blood flow resistance, and less hemolysis than the conventional silicone coil-type modules. This oxygenator was combined with the Gyro C1E3 centrifugal pump, and three ex vivo experiments were conducted to simulate pediatric V-A ECMO condition. Four day and 6 day experiments were conducted in cases 1 and 2, respectively. Case 3 was a long-term experiment up to 2 weeks. No plasma leakage and stable gas performances were achieved. The plasma free hemoglobin was maintained within a normal range. This compact pump-oxygenator system in conjunction with the Gyro C1E3 centrifugal pump has potential for a hybrid total ECMO system. [source]

Experimental Evaluation of the V-Point Heparin-Bonding System Applied to a Dense-Membrane Artificial Lung During 24-Hour Extracorporeal Circulation in Beagles

ARTIFICIAL ORGANS, Issue 8 2001
Masafumi Tashiro
Abstract: Heparin was covalently bonded to a hollow-fiber dense-membrane artificial lung and circuit using a silane coupling agent and polyethyleneimine as a spacer. This study investigated whether the novel artificial lung could sustain prolonged extracorporeal lung assist (ECLA) by venoarterial bypass in beagles using minimal anticoagulants. We maintained ECLA for 24 h in 3 groups of minimal systemic heparinization, heparinization with the new anticoagulant nafamostat mesilate, and without any systemic anticoagulant. The results were assessed from the functional performance of the artificial lung and by macroscopic and microscopic examination after the experiments. Artificial lung function, hemodynamics, hemogram, and platelet aggregation activity were well maintained in all groups. There was no plasma leakage from the artificial lung. Although several clots were observed in stagnant areas of the artificial lungs and circuits, there was no clot formation inside the artificial lung in any group. This highly biocompatible, heparin-bonded dense-membrane artificial lung performed well and safely during prolonged ECLA with blood clotting times less than 120 s. [source]

Activation of the lung S1P1 receptor reduces allergen-induced plasma leakage in mice

BRITISH JOURNAL OF PHARMACOLOGY, Issue 5 2009
F-X Blé
Background and purpose:, It has been suggested that intratracheal administration of the immunomodulator, FTY720, could have anti-inflammatory effects without causing a decrease in blood lymphocyte counts. However, the receptor responsible for this effect has not been defined. Experimental approach:, We have described, in a mouse model of allergen-induced inflammation, the use of proton magnetic resonance imaging to non-invasively assess lung fluid accumulation and inflammation. Here, we used this model to investigate the sphingosine-1-phosphate (S1P) receptor responsible for the anti-inflammatory effect of FTY720. Key results:, When given intranasally, FTY720 (3 and 10 µg·kg,1) inhibited by approximately 50% the allergen-induced accumulation of fluid in the lung detected by magnetic resonance imaging, but had no effect on the cellular inflammation in the airway space or on circulating blood lymphocytes. Inhibition of the infiltration of inflammatory cells into the airways was only observed at a dose of FTY720 that induced lymphopenia (100 µg·kg,1). Similar results were observed in S1P3 -deficient mice. The effect of FTY720 was mimicked by intranasal treatment of wild-type mice with a S1P1 -specific agonist, AUY954. Conclusions and implications:, Thus, in contrast to previously published work, our results suggest that systemic exposure of FTY720 is necessary to obtain an airway anti-inflammatory effect. On the contrary, inhibition of the allergen-induced accumulation of fluid in the lung, via activation of the S1P1 receptor, is obtainable without systemic effects. [source]