• Eur J Trauma Emerg Surg · Dec 2020

    Cerebral effects of resuscitation with either epinephrine or vasopressin in an animal model of hemorrhagic shock.

    • Jan Küchler, Stephan Klaus, Ludger Bahlmann, Nils Onken, Alexander Keck, Emma Smith, Jan Gliemroth, and Claudia Ditz.
    • Department of Neurosurgery, University of Lübeck, Ratzeburger Allee 160, 23538, Lübeck, Germany.
    • Eur J Trauma Emerg Surg. 2020 Dec 1; 46 (6): 145114611451-1461.

    PurposeThe use of epinephrine (EN) or vasopressin (VP) in hemorrhagic shock is well established. Due to its specific neurovascular effects, VP might be superior in concern to brain tissue integrity. The aim of this study was to evaluate cerebral effects of either EN or VP resuscitation after hemorrhagic shock.MethodsAfter shock induction fourteen pigs were randomly assigned to two treatment groups. After 60 min of shock, resuscitation with either EN or VP was performed. Hemodynamics, arterial blood gases as well as cerebral perfusion pressure (CPP) and brain tissue oxygenation (PtiO2) were recorded. Interstitial lactate, pyruvate, glycerol and glutamate were assessed by cerebral and subcutaneous microdialysis. Treatment-related effects were compared using one-way ANOVA with post hoc Bonferroni adjustment (p < 0.05) for repeated measures.ResultsInduction of hemorrhagic shock led to a significant (p < 0.05) decrease of mean arterial pressure (MAP), cardiac output (CO) and CPP. Administration of both VP and EN sufficiently restored MAP and CPP and maintained physiological PtiO2 levels. Brain tissue metabolism was not altered significantly during shock and subsequent treatment with VP or EN. Concerning the excess of glycerol and glutamate, we found a significant EN-related release in the subcutaneous tissue, while brain tissue values remained stable during EN treatment. VP treatment resulted in a non-significant increase of cerebral glycerol and glutamate.ConclusionsBoth vasopressors were effective in restoring hemodynamics and CPP and in maintaining brain oxygenation. With regards to the cerebral metabolism, we cannot support beneficial effects of VP in this model of hemorrhagic shock.

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