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Fibrin deposit

These steioids aie capable of preventing or suppressing the development of the sweUing, redness, local heat, and tenderness which characterize inflammation. They inhibit not only the acute symptoms of the inflammatory process, such as edema, fibrin deposition, and capillary dilatation, but also the chronic manifestations. There is evidence that glucocorticoids induce the synthesis of a protein that inhibits phosphoHpase A 2 (60), diminishing the release of arachidonic acid from phosphoHpids (Fig. 2), thereby reducing chemotaxis and inflammation. [Pg.388]

EACA muscle damage is sudden in onset and though rare is well recognized. It is uncommon when treatment involves the use of low doses below 18 g day. It usually occurs several weeks after the commencement of treatment. The drug can cause a severe necrotizing myopathy. Capillary occlusion and fibrin deposition in... [Pg.343]

A third type is a disseminated fibrin deposit in very small blood vessels or capillaries. [Pg.598]

An extended duration of therapy is required, even for susceptible pathogens, because microorganisms are enclosed within valvular vegetations and fibrin deposits. [Pg.414]

Since Lp(a) binds to fibrin, it can be directed to sites of fibrin deposition (vascular injury), providing a high concentration of cholesterol-rich lipoprotein that then can be taken up by macrophages via their scavenger receptors. This... [Pg.96]

Lipid deposition within the wall of the artery begins to intrude into the lumen If the plaque fragments at this stage, bleeding will occur leading to platelet aggregation and fibrin deposition onto the plaque. [Pg.166]

Further plaque enlargement with platelet and fibrin deposition causes severe reduction in blood flow and cells down stream become oxygen-deficient (hypoxia)... [Pg.166]

Platelet and fibrin deposition are strongly influenced by plasma and cellular factors, by properties of the vessel wall and by flow, as shown experimentally with the model of the everted deendothelialised rabbit aorta, used by Baumgartner [9]. [Pg.384]

Weiss et al. [10] have shown that platelet deposition is at a minimum at a shear rate of 50 s while fibrin deposition on subendothelium from non-anticoagulated blood is at a maximum at the same shear rate. At low shear rates (250 s ), fibrin... [Pg.384]

H.R. Baumgartner, The role of blood flow in platelet adhesion, fibrin deposition, and formation of mural thrombi, Microvasc. Res. 5(2) (1973) 167-179. [Pg.404]

Contrast MRI requires incorporation of paramagnetic material onto the PFC-based targeted particles [48,49]. Incorporation of a gadolinium(lll) complex into the lipid monolayer that coats targeted emulsion droplets provides contrast agents useful for both US and MRI modalities. Paramagnetic fibrin-specific PFC emulsion droplets allowed sensitive detection and localization of thrombi by MRI and may allow early identification of fibrin deposits in vulnerable atherosclerotic plaques. The emulsion droplets had both an antifibrin... [Pg.468]

A fibrinolytic system reverses thrombosis and thereby maintains hemostasis. Fibrinolytic enzymes and other factors work in concert to dissolve the clot using a series of rather nonspecific proteases that act locally by digesting the fibrin deposited at the site... [Pg.251]

Car BD, Suyemoto M, Neilsen NR, Slauson DO. The role of leukocytes in the pathogenesis of fibrin deposition in bovine acute lung injury, Am J Pathol 1991 ... [Pg.25]

Pierleoni C, Samuelsen GB, Graem N, Ronne E, Nielsen BS, Kaufmann P, et al. Immu-nohistochemical identification of the receptor for urokinase plasminogen activator associated with fibrin deposition in normal and ectopic human placenta. Placenta 1998 19(7) 501-508. [Pg.96]

Healy AM, Hancock WW, Christie PD et al. (1998) Intravascular coagulation activation in a murine model of thrombomodulin deficiency effects of lesion size, age, and hypoxia on fibrin deposition. Blood 92 4188-4197 Weiler-Guettler H, Christie PD, Beeler DL et al. (1998) A targeted point mutation in thrombomodulin generates viable mice with a prethrombotic state. J Clin Invest 101 1983-1991... [Pg.306]

Normal fertility, viability and development no bleeding disorder spontaneous lysis of injected clots -> enhanced fibrinolytic potential significant reduction of renal fibrin deposition after LPS (Lijnen et al. 1999). [Pg.307]

Extensive spontaneous fibrin deposition severe spontaneous thrombosis impaired neointima formation reduced ovulation and fertility cachexia and shorter survival severe glomerulonephritis abnormal tissue remodelling (Carmeliet et al. 1994 Christie et al. 1999). [Pg.307]

Pinsky DJ, Liao H, Lawson CA et al. (1998) Coordinated induction of plasminogen activator inhibitor-1 (PAI-1) and inhibition of plasminogen activator gene expression by hypoxia promotes pulmonary vascular fibrin deposition. J Clin Invest 102 919-928... [Pg.307]

Single u-PA deficiency viable, fertile, normal life span occasionally spontaneous fibrin deposits in normal and inflamed tissue higher incidence of endotoxin-induced thrombosis. Combined t-PA and u-PA deficiency mice survive embryonic development retarded growth, reduced fertility, shortened life span spontaneous fibrin deposits more extensively and in more organs (Carmeliet et al. 1994 Heckel et al. 1990). [Pg.307]

Experimental studies in perfusion devices can also be performed with non-anticoagulated blood [52] or with blood anticoagulated with low molecular weight heparin [53]. In contrast with the studies with citrated blood, the latter experimental systems allow the generation of thrombin and fibrin deposition on the damaged vessel due the concurrence of several mechanisms exposure of tissue fector in the subendothelium [54], presence of plasma coagulation fectors [55] and the expression of a procoagulant surface on activated platelets. [Pg.349]

Salatti JA, FenUm J, Anton P, Sakariassen KS alpha-Thrombin bound to extracdlular endothelial matrix induces pronounced fibrin deposition and platelet thrombus growth in flowing non-antiooagulated human blood. Blood Coagul Fibrin 5 561-566,1994. [Pg.358]

Glucocorticoids inhibit pathways that normally lead to production of prostaglandins, leukotrienes and platelet activating factor. These mediators would normally contribute to increased vascular permeability and subsequent changes including oedema, leucocyte migration, fibrin deposition. [Pg.664]

Fig. 25.19 Laparoscopic view of a large Echinococcus cysticus hydatid in the right lobe of liver irregularly thickened hypervascu-lar capsule. Fibrin deposition at the adjacent peritoneum. Distended elastic consistency... Fig. 25.19 Laparoscopic view of a large Echinococcus cysticus hydatid in the right lobe of liver irregularly thickened hypervascu-lar capsule. Fibrin deposition at the adjacent peritoneum. Distended elastic consistency...
Skin-test reactivity, that is induration and tissue factor generation by monocjdes, is reduced by therapeutic doses of oral anticoagulants, but Ijmphocyte transformation activity is not. This constitutes the rationale for the use of oral anticoagulants in the treatment of immune diseases characterized by fibrin deposition, such as allograft rejection and lupus nephritis (70). [Pg.987]

Figure 3. Mitomycin C induced thrombotic microangiopathy. Glomeruli show swelling and detatchment of endothelial cells and luminal occlusion. The arterioles and arteries show intimal cellular swelling and hyperplasia and fibrin deposition. Masson s trichrome staining, magn. x325. Figure 3. Mitomycin C induced thrombotic microangiopathy. Glomeruli show swelling and detatchment of endothelial cells and luminal occlusion. The arterioles and arteries show intimal cellular swelling and hyperplasia and fibrin deposition. Masson s trichrome staining, magn. x325.

See other pages where Fibrin deposit is mentioned: [Pg.492]    [Pg.108]    [Pg.997]    [Pg.142]    [Pg.160]    [Pg.165]    [Pg.593]    [Pg.689]    [Pg.385]    [Pg.131]    [Pg.12]    [Pg.281]    [Pg.23]    [Pg.16]    [Pg.129]    [Pg.67]    [Pg.297]    [Pg.303]    [Pg.310]    [Pg.588]    [Pg.565]    [Pg.6]   
See also in sourсe #XX -- [ Pg.598 ]




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