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Related Experiment Videos

Tissue factor in experimental acute lung injury.

K E Welty-Wolf1, M S Carraway, S Idell

  • 1Division of Pulmonary and Critical Care Medicine, Department of Medicine, Duke University and Durham Veterans Affairs Medical Centers, Durham, NC 27710, USA.

Seminars in Hematology
|December 6, 2001
PubMed
Summary

Blocking tissue factor (TF)-initiated coagulation with FVIIai in sepsis-induced acute lung injury (ALI) reduced fibrin deposition, inflammation, and edema. This intervention improved lung function and organ recovery, highlighting TF-FVIIa as a key therapeutic target.

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Area of Science:

  • Pulmonary Medicine
  • Hematology
  • Critical Care

Background:

  • Acute lung injury (ALI) involves fibrin deposition and a procoagulant state in the lungs, often linked to endotoxin or bacterial exposure.
  • Tissue factor (TF)-dependent coagulation activation and increased inflammatory cytokines are characteristic of sepsis-induced ALI and acute respiratory distress syndrome (ARDS).
  • The precise role of TF in regulating pulmonary inflammatory responses during sepsis remains incompletely understood.

Purpose of the Study:

  • To investigate the therapeutic potential of blocking TF-initiated coagulation in a baboon model of Escherichia coli sepsis-induced ALI.
  • To evaluate the effects of active site-inactivated FVIIa (FVIIai) on coagulation, inflammation, and organ function in sepsis-induced ALI.

Main Methods:

  • Baboons with Escherichia coli sepsis-induced ALI were treated with active site-inactivated FVIIa (FVIIai).

Related Experiment Videos

  • Evaluated effects on plasma fibrinogen, tissue fibrin deposition, systemic cytokine levels, lung neutrophil infiltration, edema, gas exchange, compliance, pulmonary hypertension, and renal function.

    • Main Results:

    • FVIIai treatment prevented plasma fibrinogen depletion and reduced fibrin deposition in lung tissues.
    • The blockade attenuated systemic cytokine responses, decreased lung inflammation (including neutrophil infiltration), and reduced edema.
    • Coagulation blockade with FVIIai improved lung function (gas exchange, compliance), decreased pulmonary hypertension, and enhanced renal function.

    Conclusions:

    • The TF-FVIIa complex is a critical regulatory point in the lung's pathological response to sepsis.
    • Blocking TF-initiated coagulation with FVIIai demonstrates significant therapeutic benefits in sepsis-induced ALI, improving both lung and systemic organ function.
    • These findings support TF-FVIIa as a promising target for treating ALI and ARDS associated with sepsis.