Fibrin degradation products increase lung transvascular fluid filtration after thrombin-induced pulmonary microembolism

Johnson, A.; Garcia-Szabo, R. R.; Kaplan, John E.; Malik, Asrar B.

doi:10.1016/0049-3848(85)90100-8

Cited by 17 publications

(12 citation statements)

References 15 publications

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“…Pulmonary microvascular thrombosis was described in septic patients three decade ago (56). Malik et al (57)(58)(59)(60) clearly demonstrated that intravascular thrombin, fibrin, and neutrophils interacted synergistically to increase lung endothelial permeability to protein. It is now accepted that DICassociated microvascular thrombosis, together with neutrophil-endothelial activation, and secondary endothelial injury contribute to the initiation, course, and prognosis of acute lung injury/acute respiratory distress syndrome (61).…”

Section: Microvascular Thrombosis and Organ Dysfunctionmentioning

confidence: 98%

Microvascular thrombosis and multiple organ dysfunction syndrome

Gando¹

2010

Critical Care Medicine

281

147

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This paper will review the involvement of disseminated intravascular coagulation-induced microvascular thrombosis in the pathogenesis of multiple organ dysfunction syndrome and the interaction between disseminated intravascular coagulation and systemic inflammatory response syndrome in critically ill patients. The published literature on clinical and experimental studies are the data sources of the study. Histologic evidence of microvascular thrombosis and tissue injury in disseminated intravascular coagulation has been reported in clinical, experimental, and autopsy findings. Proinflammatory cytokine-evoked neutrophil-endothelial activation and interplay between inflammation and coagulation through protease-activated receptors contribute to enhanced microvascular fibrin deposition in organs. In a clinical setting, systemic inflammatory response syndrome and disseminated intravascular coagulation synergistically play pivotal roles in the development of multiple organ dysfunction syndrome and in the poor prognosis of critical illness. Disseminated intravascular coagulation contributes to microvascular thrombosis and subsequent multiple organ dysfunction syndrome. Recent knowledge on the relationship between disseminated intravascular coagulation and systemic inflammatory response syndrome gives further insight into the pathogenic mechanisms of multiple organ dysfunction syndrome in critically ill patients.

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Section: Microvascular Thrombosis and Organ Dysfunctionmentioning

confidence: 98%

Microvascular thrombosis and multiple organ dysfunction syndrome

Gando¹

2010

Critical Care Medicine

281

147

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“…It is also conceivable, however, that less fibrin generation in the presence of hirudin resulted in less generation of fibrin degradation products (FDP). FDP released after the action of plasmin on fibrin are thought to contribute to the development of acute lung injury by increasing the permeability of the lung vasculature to protein (21,42). We have previously shown that the infusion of a fibrin-derived peptide into pigs causes an increase in EVLW (43).…”

Section: Discussionmentioning

confidence: 99%

Effect of Recombinant Hirudin, a Specific Inhibitor of Thrombin, on Endotoxin-induced Intravascular Coagulation and Acute Lung Injury in Pigs

Hoffmann¹,

Siebeck²,

Spannagl³

et al. 1990

Am Rev Respir Dis

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“…Although digestion of Fg by plasmin in vivo is quite rare (Boutcher et al. 1996, Gaffney 2001), increased vascular permeability has been found to result from the interaction of thrombin and Fg (Johnson et al. 1983, 1985).…”

Section: Effects Of Fg In the Microcirculationmentioning

confidence: 99%

“…Infusion of fragment D into conscious rabbits increased vascular permeability to albumin (Manwaring & Curreri 1981). However, another study showed that infusion of fragment D alone in sheep did not alter pulmonary transvascular fluid and protein exchange (Johnson et al. 1985).…”

Section: Effects Of Fg In the Microcirculationmentioning

confidence: 99%

Mechanisms of fibrinogen‐induced microvascular dysfunction during cardiovascular disease

et al. 2009

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Fibrinogen (Fg) is a high molecular weight plasma adhesion protein and a biomarker of inflammation. Many cardiovascular and cerebrovascular disorders are accompanied by increased blood content of Fg. Increased levels of Fg result in changes in blood rheological properties such as increases in plasma viscosity, erythrocyte aggregation, platelet thrombogenesis, alterations in vascular reactivity and compromises in endothelial layer integrity. These alterations exacerbate the complications in peripheral blood circulation during cardiovascular diseases such as hypertension, diabetes and stroke. In addition to affecting blood viscosity by altering plasma viscosity and erythrocyte aggregation, growing experimental evidence suggests that Fg alters vascular reactivity and impairs endothelial cell layer integrity by binding to its endothelial cell membrane receptors and activating signalling mechanisms. The purpose of this review is to discuss experimental data, which demonstrate the effects of Fg causing vascular dysfunction and to offer possible mechanisms for these effects, which could exacerbate microcirculatory complications during cardiovascular diseases accompanied by increased Fg content.

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Fibrin degradation products increase lung transvascular fluid filtration after thrombin-induced pulmonary microembolism

Cited by 17 publications

References 15 publications

Microvascular thrombosis and multiple organ dysfunction syndrome

Microvascular thrombosis and multiple organ dysfunction syndrome

Effect of Recombinant Hirudin, a Specific Inhibitor of Thrombin, on Endotoxin-induced Intravascular Coagulation and Acute Lung Injury in Pigs

Mechanisms of fibrinogen‐induced microvascular dysfunction during cardiovascular disease

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