Early hemorrhage triggers metabolic responses that build up during prolonged shock.

摘要: Metabolic staging after trauma/hemorrhagic shock is a key driver of acidosis and directly relates to hypothermia coagulopathy. responses have been assayed through classic biochemical approaches or NMR, thereby lacking comprehensive overview the dynamic metabolic changes occurring shock. Sprague-Dawley rats underwent progressive hemorrhage Baseline postshock blood was collected, late hyperfibrinolysis assessed (LY30 >3%) in all tested rats. Extreme intermediate time points were collected assay plasma metabolome via ultra-high performance liquid chromatography-mass spectrometry. Sham controls used determine whether could be primarily attributable anesthesia supine positioning. Early hemorrhage-triggered that built up progressively became significant during sustained hemorrhagic phenotypes either resulted immediate hypercatabolism, preceded by deregulation early subset Hemorrhagic consistently promoted hyperglycemia, glycolysis, Krebs cycle, fatty acid, amino nitrogen metabolism (urate polyamines), impaired redox homeostasis. are triggered Future studies will subphenotypes observed might humans pave way for tailored resuscitative strategies.