Max Roy1, Manuel Burggraf1, Sven Lendemans1, Herbert de Groot2, Ricarda Rohrig3. 1. Department for Orthopedics and Emergency Surgery, University Hospital Essen, Essen, Germany. 2. Institute of Physiological Chemistry, University Hospital Essen, Essen, Germany. 3. Institute of Physiological Chemistry, University Hospital Essen, Essen, Germany. Electronic address: ricarda.rohrig@uk-essen.de.
Abstract
BACKGROUND: The plasmin/plasminogen inhibitor tranexamic acid (TXA) is mainly used in elective surgeries with a higher blood loss to avoid uncontrolled bleeding. Recently, TXA has also been shown to reduce mortality in trauma patients. It is assumed that its beneficial effects are principally caused by its antifibrinolytic properties. We hypothesize that TXA also improves survival in a modified Wigger's model of hemorrhagic shock by a mechanism other than antifibrinolysis. MATERIALS AND METHODS: Male Wistar rats were intermittently bled until the mean arterial blood pressure was dropped to 25-30 mm Hg (severe shock). After shock induction, the animals received either 0.14-0.15 mL TXA (30 mg/kg) i.v. or the equivalent volume of 0.9% NaCl given as bolus. Adjacent to the shock period, the rats were resuscitated with Ringer's solution within 30 min and observed for another 150 min unless the animals died earlier. RESULTS: In the animals treated with TXA, survival was clearly prolonged and acid-base parameters showed some differences as compared to the animals receiving only NaCl. In the model used, coagulation slightly declined, but an increased fibrinolysis was not observed. CONCLUSIONS: Since in the applied shock model fibrinolysis is negligible, we postulate that TXA is capable of providing protection against hemorrhagic shock independent from its antifibrinolytic properties.
BACKGROUND: The plasmin/plasminogen inhibitor tranexamic acid (TXA) is mainly used in elective surgeries with a higher blood loss to avoid uncontrolled bleeding. Recently, TXA has also been shown to reduce mortality in traumapatients. It is assumed that its beneficial effects are principally caused by its antifibrinolytic properties. We hypothesize that TXA also improves survival in a modified Wigger's model of hemorrhagic shock by a mechanism other than antifibrinolysis. MATERIALS AND METHODS: Male Wistar rats were intermittently bled until the mean arterial blood pressure was dropped to 25-30 mm Hg (severe shock). After shock induction, the animals received either 0.14-0.15 mL TXA (30 mg/kg) i.v. or the equivalent volume of 0.9% NaCl given as bolus. Adjacent to the shock period, the rats were resuscitated with Ringer's solution within 30 min and observed for another 150 min unless the animals died earlier. RESULTS: In the animals treated with TXA, survival was clearly prolonged and acid-base parameters showed some differences as compared to the animals receiving only NaCl. In the model used, coagulation slightly declined, but an increased fibrinolysis was not observed. CONCLUSIONS: Since in the applied shock model fibrinolysis is negligible, we postulate that TXA is capable of providing protection against hemorrhagic shock independent from its antifibrinolytic properties.
Authors: Patrick F Walker; Anthony D Foster; Philip A Rothberg; Thomas A Davis; Matthew J Bradley Journal: PLoS One Date: 2018-11-29 Impact factor: 3.240