In Vitro Pleural Fluid Clottability and Fibrinogen Content

Glauser, Frederick L.; Otis, Peter T.; Levine, Richard I.; Smith, William R.

doi:10.1378/chest.68.2.205

Cited by 13 publications

(7 citation statements)

References 7 publications

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“…Similar trends of procoagulant and fibrinolytic activities occurred in association with exudative pleural disease, indicating that locally disordered fibrin turnover is not specific to the alveolar space in DAD but may also accompany exudative processes in the pleural compartment. The lack of consistently increased procoagulant activity in empyema fluids is consistent with previous reports (41) and indicates that high-grade inflammation in the pleural space is not invariably associated with increased local procoagulant activity, such as consistently occurs in BAL during evolving DAD.…”

Section: Discussionsupporting

confidence: 90%

Local abnormalities of coagulation and fibrinolytic pathways that promote alveolar fibrin deposition in the lungs of baboons with diffuse alveolar damage.

Idell¹,

Peters²,

James³

et al. 1989

J. Clin. Invest.

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Because alveolar fibrin is a prominent histologic feature of diffuse lung injury in baboons, we hypothesized that local abnormalities of pathways of fibrin turnover would favor fibrin deposition in the alveolar space. To test this hypothesis, procoagulant and fibrinolytic activities were characterized in serial bronchoalveolar lavage (BAL) of baboons with evolving diffuse alveolar damage (DAD) induced by exposure to 100% 02. BAL procoagulant activity, characterized mainly as the tissue factor-Factor VII complex, was markedly increased after induction of DAD. Extrinsic pathway inhibitor was likewise increased in BAL during evolving DAD but was insufficient to control coagulation. Urokinase-like fibrinolytic activity was usually detectable in baseline BAL but was undetectable after 7 d of 02. DAD BAL contained significantly increased plasminogen levels, plasmin inhibitor activity sufficient to neutralize all plasmin produced by BAL plasminogen activator found in control BAL and detectable plasminogen activator inhibitor-i. Antiplasmin activity was due, in part, to increased a2-antiplasmin. These changes correlated with quantitatively increased alveolar fibrin deposition demonstrated by histologic and morphometric analyses. Multiple abnormalities of pathways of fibrin turnover occur concurrently in the alveolar compartment of the lungs of baboons with DAD, which collectively predispose to diffuse alveolar fibrin deposition.

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Section: Discussionsupporting

confidence: 90%

Local abnormalities of coagulation and fibrinolytic pathways that promote alveolar fibrin deposition in the lungs of baboons with diffuse alveolar damage.

Idell¹,

Peters²,

James³

et al. 1989

J. Clin. Invest.

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“…This latter hypothesis would explain the few pleural effusions with increased FDPs but with D-dimer concentrations lower than the plasma reference interval or lower compared to their corresponding plasma value. Similar conclusions have been reached by experiments in a canine model [ 27 , 37 ] and in the human clinical setting [ 38 – 40 ].…”

Section: Discussionsupporting

confidence: 85%

Hemostatic findings of pleural fluid in dogs and the association between pleural effusions and primary hyperfibrino(geno)lysis: A cohort study of 99 dogs

et al. 2018

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The primary objective of this study was to determine if activation of coagulation and fibrinolysis occurs in canine pleural effusions. Thirty-three dogs with pleural effusions of different origin were studied. Pleural effusion fibrinogen concentrations were significantly lower, while pleural fibrin-fibrinogen degradation products (FDPs) and D-dimer concentrations were significantly higher than those in plasma (P < 0.001 for all comparisons). These results show that, in canine pleural fluids, there is evidence of coagulation activation and fibrinolysis. The secondary aims of the current study were to determine if primary hyperfibrinolysis ([PHF] i.e., elevated plasma FDPs with a normal D-dimer concentrations), occurs in dogs with pleural effusion, and whether the presence of a concurrent inflammatory process may have activated the hemostatic cascade, with its intrinsically linked secondary hyperfibrinolysis, masking the concurrent PHF. The previously 33 selected dogs with pleural effusion (group 1) were compared to two control groups of 33 healthy (group 2) and 33 sick dogs without pleural effusion (group 3). Serum fibrinogen, FDPs, D-dimer, C-reactive protein (CRP), fibrinogen/CRP ratio, and frequency of PHF were determined. Fibrinogen, FDPs, D-dimer and CRP concentrations in group 1 were significantly increased compared to group 2 (P < 0.001 for all comparisons). FDPs and CRP concentrations in group 1 were also significantly increased compared to group 3 (P = 0.001 and P < 0.001, respectively). The fibrinogen/CRP ratio was significantly decreased in group 1 compared to groups 2 and 3 (P < 0.001 for both comparison). The frequency of PHF was significantly higher in group 1 compared to groups 2 (P = 0.004), but not compared to group 3. These results support the hypothesis that PHF occurs significantly more often in dogs with pleural effusion compared to healthy dogs. Nevertheless, the decrease in the fibrinogen/CRP ratio in group 1 compared to group 3, considering the higher FDPs and similar D-dimer concentrations, would suggest that PHF is also more frequent in dogs with pleural effusion compared to sick control dogs, and that this phenomenon is hidden due to concurrent secondary hyperfibrinolysis.

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“…The mesothelium expresses components of both procoagulant and fibrinolytic pathways [10,42,43] and the local equilibrium between their activities is critical for homeostatic control of fibrin generation and turnover in the pleural space [4]. Most types of pleural injury disrupt this equilibrium towards the procoagulant side, leading to fibrin deposition in the pleural space.…”

Section: Discussionmentioning

confidence: 99%

Plasmin enhances cell surface tissue factor activity in mesothelial and endothelial cells

Kothari

Kaur

Sahoo

et al. 2009

Journal of Thrombosis and Haemostasis

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Summary. Background: Mesothelial cells that line the thoracic cavity play an important role in maintaining the local balance between procoagulant and fibrinolytic activity, a role akin to the endothelial cells in blood vessels. The mechanism(s) responsible for increased tissue factor (TF) expression in mesothelial cells in response to injury are at present unclear. Objective: To investigate whether plasmin or thrombin, two major proteases that may be generated on the pleural surface upon injury, induce TF expression in human pleural mesothelial cells (HMC) and elucidate the underlying mechanism(s). Methods: Confluent monolayers of HMC and human umbilical vein endothelial cells (HUVEC) were exposed to plasmin or thrombin for varying time periods and TF expression was analyzed by measuring its activity in a factor Xa generation assay, TF antigen levels by immunoblot analysis and TF mRNA by Northern blot analysis. Results: Both plasmin and thrombin treatments increased cell surface TF activity in HMC by 3-to 4-fold. In contrast to thrombin, plasmin-induced TF activity is not dependent on the de novo synthesis of TF. In HUVEC, plasmin had a minimal effect on unperturbed HUVEC whereas it markedly increased TF activity of activated HUVEC. Plasmin treatment neither affected anionic phospholipid levels at the cell surface nor released protein disulfide isomerase, an oxidoreductase protein that was newly described to play a role in TF activation. Plasmin cleaved cell-associated TFPI. Conclusion: Thrombin up-regulates TF activity in HMC through the transcriptional activation of TF whereas plasmin increases TF activity by inactivating the cell-associated TFPI by a limited proteolysis.

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In Vitro Pleural Fluid Clottability and Fibrinogen Content

Cited by 13 publications

References 7 publications

Local abnormalities of coagulation and fibrinolytic pathways that promote alveolar fibrin deposition in the lungs of baboons with diffuse alveolar damage.

Local abnormalities of coagulation and fibrinolytic pathways that promote alveolar fibrin deposition in the lungs of baboons with diffuse alveolar damage.

Hemostatic findings of pleural fluid in dogs and the association between pleural effusions and primary hyperfibrino(geno)lysis: A cohort study of 99 dogs

Plasmin enhances cell surface tissue factor activity in mesothelial and endothelial cells

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