January 6, 2016BloodOpen Access

A systems approach to hemostasis: 4. How hemostatic thrombi limit the loss of plasma-borne molecules from the microvasculature

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Population

Mouse cremaster muscle venules subjected to penetrating injuries

Design

Preclinical

Authors

JWJohn D. WelshUniversity of Pennsylvania RMRyan W. MuthardUniversity of Pennsylvania TSTimothy J. StalkerThomas Jefferson University

Discussion

Member takes

Implication

Thrombus core-shell architecture may enhance plasma sealing beyond red cell containment; leaves open whether antithrombotics meaningfully alter clinical bleeding risk.

Structured PICO

Population

Mouse cremaster muscle venules subjected to penetrating injuries

Intervention

Antiplatelet agents (αIIbβ3 antagonist, ADP P2Y12 receptor inhibitors), reduced integrin-dependent signaling, hirudin, or Gi2α gain-of-function mutation

Outcome

Vessel sealing and extravascular protein accumulation measured by intravital microscopy with a photo-activatable fluorescent albumin markersurrogate

In a mouse model of microvascular injury, stable platelet accumulation and ADP-dependent signaling, rather than fibrin accumulation, are the critical events for limiting plasma extravasation.

Cite This Study

Welsh et al. (2016) studied this question.

synapsesocial.com/papers/6a702715e5469ee92be0ea79 https://doi.org/10.1182/blood-2015-09-672188

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Implication

Thrombus core-shell architecture may enhance plasma sealing beyond red cell containment; leaves open whether antithrombotics meaningfully alter clinical bleeding risk.