Oxygenation extremes after traumatic brain injury transiently affect coagulation
| Autor: | Amy T. Makley, Michael D. Goodman, Rosalie Veile, Mackenzie C. Morris, Lou Ann Friend, Kathleen E. Singer, Emily McGlone, Grace M. Niziolek |
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| Rok vydání: | 2019 |
| Předmět: |
Hyperoxia
Platelet Aggregation Platelet Function Tests business.industry Traumatic brain injury Hematology Oxygenation Hypoxia (medical) medicine.disease Thrombelastography Thromboelastometry Mice Clotting time Anesthesia Brain Injuries Traumatic Coagulopathy medicine Animals Humans Platelet medicine.symptom business Blood Coagulation |
| Zdroj: | Thrombosis research. 186 |
| ISSN: | 1879-2472 |
| Popis: | Introduction Trauma patients may become hypoxic or iatrogenically hyperoxic in the early post-injury period. While both extremes of oxygenation may be harmful following injury, the mechanism has yet to be elucidated. We hypothesized that hypoxia or hyperoxia would induce changes in coagulation, creating a secondary insult exacerbating the primary injury. Materials and methods Mice underwent traumatic brain injury (TBI) or sham and were subsequently exposed to room air or brief hypoxia (15% FiO2) then sacrificed at intervals. Another cohort of uninjured mice underwent more prolonged hypoxia (10% FiO2) or hyperoxia (60% FiO2). Platelet function was evaluated by ADP- or ASPi-induced impedance aggregometry and viscoelastic coagulation parameters were assessed with rotational thromboelastometry. Results In uninjured mice, ADP-induced platelet aggregation was acutely increased after prolonged hypoxia, but this difference did not persist at 6 h. Hypoxic and hyperoxic TBI mice had increased ADP induced platelet aggregation at 1 h compared to the normoxia group. TBI mice demonstrated an early increased platelet aggregation after hypoxia or hyperoxia. Viscoelastic coagulation parameters were similar between hypoxic, hyperoxic and room air groups at 1 h and 6 h. However, ROTEM clotting time and clot formation time were prolonged and maximal clot firmness were lower in sham TBI/hypoxia mice at 24 h. Conclusion Post-TBI hypoxia and hyperoxia resulted in transiently increased platelet aggregation in response to ADP, without lasting effecting on platelet function or coagulation. Hypoxia also induced delayed hypocoagulability after platelet aggregation normalized. Brief changes in oxygenation may temporally affect coagulation and platelet aggregation, which could contribute to physiologic secondary injury after trauma. |
| Databáze: | OpenAIRE |
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