ArticleSurgery2015
Fibrinolysis shutdown phenotype masks changes in rodent coagulation in tissue injury versus hemorrhagic shock.
Article in Surgery, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 73 citations in OpenAlex.
- Characterization of the binding of skeletal muscle myosin to fibrin in trauma.The journal of trauma and acute care surgery · 2026Article
- From molecular networks to precision therapeutics: the evolving landscape of trauma-induced coagulopathy.World journal of emergency surgery : WJES · 2026Review
- Change in novel plasmin activated clotting time assay predicts hyperfibrinolysis, massive transfusion, and mortality in trauma in under 3 minutes.American journal of surgery · 2025Article
- Trauma-Induced Coagulopathy: A Review of Specific Molecular Mechanisms.Diagnostics (Basel, Switzerland) · 2025Review
- Liquid biopsy in orthopedic trauma: exosomes as functional mediators and mechanistic indicators in post-traumatic complications.Frontiers in medicine · 2025Review
- Phenotypes of Disseminated Intravascular Coagulation.Thrombosis and haemostasis · 2024Article
- Hemorrhagic shock and tissue injury provoke distinct components of trauma-induced coagulopathy in a swine model.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2023Article
- SHock-INduced Endotheliopathy (SHINE): A mechanistic justification for viscoelastography-guided resuscitation of traumatic and non-traumatic shock.Frontiers in physiology · 2023Review
- The efficacy of tranexamic acid treatment with different time and doses for traumatic brain injury: a systematic review and meta-analysis.Thrombosis journal · 2022Article
- Acute mesenteric ischemia: updated guidelines of the World Society of Emergency Surgery.World journal of emergency surgery : WJES · 2022Review
- Correlation between Coagulation Fibrinolysis Function and Outcomes during Hospitalization in Patients with Severe Traumatic Hemorrhagic Shock.Emergency medicine international · 2022Article
- The Pathophysiology and Management of Hemorrhagic Shock in the Polytrauma Patient.Journal of clinical medicine · 2021Review
- Early abnormal fibrinolysis and mortality in patients with thermal injury: a prospective cohort study.BJS open · 2021Observational
- 28-day thawed plasma maintains αVox sanguinis · 2021Article
- Detection of early allograft dysfunction at 30 min of reperfusion in liver transplantation: An intraoperative diagnostic tool with real time assessment of graft function.American journal of surgery · 2020Article
- A rat model of orthopedic injury-induced hypercoagulability and fibrinolytic shutdown.The journal of trauma and acute care surgery · 2020Article
- Actin is associated with tissue injury in trauma patients and produces a hypercoagulable profile in vitro.The journal of trauma and acute care surgery · 2020Article
- High Rate of Fibrinolytic Shutdown and Venous Thromboembolism in Patients With Severe Pelvic Fracture.The Journal of surgical research · 2020Article
- Fibrinolysis Shutdown in Trauma: Historical Review and Clinical Implications.Anesthesia and analgesia · 2019Review
- Does Tranexamic Acid Improve Clot Strength in Severely Injured Patients Who Have Elevated Fibrin Degradation Products and Low Fibrinolytic Activity, Measured by Thrombelastography?Journal of the American College of Surgeons · 2019Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
introductionSystemic hyperfibrinolysis (accelerated clot degradation) and fibrinolysis shutdown (impaired clot degradation) are associated with increased mortality compared with physiologic fibrinolysis after trauma. Animal models have not reproduced these changes. We hypothesize rodents have a shutdown phenotype that require an exogenous profibrinolytic to differentiate mechanisms that promote or inhibit fibrinolysis.
methodsFibrinolysis resistance was assessed by thrombelastography (TEG) using exogenous tissue plasminogen activator (tPA) titrations in whole blood. There were 3 experimental groups: (1) tissue injury (laparotomy/bowel crush), (2) shock (hemorrhage to mean arterial pressure of 20 mmHg), and (3) control (arterial cannulation and tracheostomy). Baseline and 30-minute postintervention blood samples were collected, and assayed with TEG challenged with taurocholic acid (TUCA).
resultsRats were resistant to exogenous tPA; the percent clot remaining 30 minutes after maximum amplitude (CL30) at 150 ng/mL (P = .511) and 300 ng/mL (P = .931) was similar to baseline, whereas 600 ng/mL (P = .046) provoked fibrinolysis. Using the TUCA challenge, the percent change in CL30 from baseline was increased in tissue injury compared with control (P = .048.), whereas CL30 decreased in shock versus control (P = .048). tPA increased in the shock group compared with tissue injury (P = .009) and control (P = .012).
conclusionRats have an innate fibrinolysis shutdown phenotype. The TEG TUCA challenge is capable of differentiating changes in clot stability with rats undergoing different procedures. Tissue injury inhibits fibrinolysis, whereas shock promotes tPA-mediated fibrinolysis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.