Non-human primate model of poly-traumatic hemorrhagic shock recapitulates early platelet dysfunction observed following severe injury in humans.

Background: Platelet dysfunction has been described as an early component of trauma induced coagulopathy (TIC). The platelet component of TIC remains to be fully elucidated and translatable animal models are required to facilitate mechanistic investigations. We sought to determine if the early platelet dysfunction described in trauma patients could be recapitulated in an non-human primate (NHP) model of poly-traumatic hemorrhagic shock. Methods: Twenty-four male Rhesus Macaques weighting 7-14 kilograms were subjected to 60 minutes (min) severe pressure-targeted controlled hemorrhagic shock (HS) with and without other injuries. After 60min, resuscitation with 0.9% NaCl and whole blood was initiated. Platelet counts and platelet aggregation assays were performed at baseline (BSLN), end of shock (T=60min, EOS), end of resuscitation (T=180min, EOR), and T=360min on overall cohort. Results are reported as mean+/-standard deviation (SD) or median (interquartile range). Statistical analysis was conducted using Spearmen correlation, one-way ANOVA, two-way RM-ANOVA, paired t-test or Wilcoxon non-parametric test, with p

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