ArticleThe Journal of surgical research2015
Shock releases bile acid inducing platelet inhibition and fibrinolysis.
Article in The Journal of surgical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Validation of the BEST-J score and identification of bile reflux as a risk factor for delayed bleeding after gastric endoscopic submucosal dissection.BMC gastroenterology · 2026Article
- High-Throughput Metabolomics in Transfusion Medicine.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Discovery and Functional Validation of EP3 Receptor Ligands with Therapeutic Potential in Cardiovascular Disease.International journal of molecular sciences · 2025Article
- Metabolic signatures of cardiorenal dysfunction in plasma from sickle cell patients as a function of therapeutic transfusion and hydroxyurea treatment.Haematologica · 2023Article
- Red Blood Cell Omics and Machine Learning in Transfusion Medicine: Singularity Is Near.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2023Review
- "Importance of catecholamine signaling in the development of platelet exhaustion after traumatic injury": Reply.Journal of thrombosis and haemostasis : JTH · 2022Article
- Importance of catecholamine signaling in the development of platelet exhaustion after traumatic injury.Journal of thrombosis and haemostasis : JTH · 2022Article
- Retention of functional mitochondria in mature red blood cells from patients with sickle cell disease.British journal of haematology · 2022Article
- Irradiation Causes Alterations of Polyamine, Purine, and Sulfur Metabolism in Red Blood Cells and Multiple Organs.Journal of proteome research · 2022Article
- Changes of farnesoid X receptor and Takeda G-protein coupled receptor 5 following biliary tract external drainage in hemorrhagic shock.Experimental and therapeutic medicine · 2022Article
- Gut microbiota and derived metabolomic profiling in glaucoma with progressive neurodegeneration.Frontiers in cellular and infection microbiology · 2022Article
- Observational
- Biological and Clinical Factors contributing to the Metabolic Heterogeneity of Hospitalized Patients with and without COVID-19.Research square · 2021Article
- Decreased Physiological Serum Total Bile Acid Concentrations in Patients with Type 2 Diabetic Peripheral Neuropathy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- Selective organ ischaemia/reperfusion identifies liver as the key driver of the post-injury plasma metabolome derangements.Blood transfusion = Trasfusione del sangue · 2019Article
- Increase in post-reperfusion sensitivity to tissue plasminogen activator-mediated fibrinolysis during liver transplantation is associated with abnormal metabolic changes and increased blood product utilisation.Blood transfusion = Trasfusione del sangue · 2019Article
- Trauma-induced coagulopathy: The past, present, and future.Journal of thrombosis and haemostasis : JTH · 2019Review
- Hemorrhagic shock and tissue injury drive distinct plasma metabolome derangements in swine.The journal of trauma and acute care surgery · 2017Article
- Red blood cells in hemorrhagic shock: a critical role for glutaminolysis in fueling alanine transamination in rats.Blood advances · 2017Article
- Farnesoid X Receptor and Its Ligands Inhibit the Function of Platelets.Arteriosclerosis, thrombosis, and vascular biology · 2016Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundMetabolites are underappreciated for their effect on coagulation. Taurocholic acid (TUCA), a bile acid, has been shown to regulate cellular activity and promote fibrin sealant degradation. We hypothesize that TUCA impairs whole blood clot formation and promotes fibrinolysis.
methodsTUCA was exogenously added to whole blood obtained from volunteers. A titration from 250 μM-750 μM was used due to biologic relevance. Whole blood mixtures were assayed using thrombelastography for clot strength (maximum amplitude [MA]) and fibrinolysis (LY30) quantification. Tranexamic acid was used to block plasmin-mediated fibrinolysis. Platelet microfluidics were performed. A proteomic analysis was completed on citrated plasma obtained from a shock and resuscitation rat model.
resultsFibrinolysis increased when 750-μM TUCA was added to whole blood (median LY30 0.08-5.7, P = 0.010) and clot strength decreased (median MA of 53.3-43.8, P = 0.010). The addition of tranexamic acid, to a 750-μM TUCA titration, partially reversed the induced fibrinolysis (LY30: without 7.7 versus with 2.7) and the decrease in clot strength (MA: without 48.2 versus with 53.2), but did not reverse the effects to whole blood levels. Platelet function reduced by 50% in the presence of 100-μM TUCA. Rats had a median 52-fold increase in TUCA, after a shock state that stayed elevated after resuscitation.
conclusionsTUCA reduces clot strength and promotes fibrinolysis. The clot strength reduction is attributable to platelet inhibition. This metabolic effect on coagulation warrants further investigation, as localized areas of the body, with high levels of bile acid, may be at risk for postoperative bleeding.
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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.