Tissue injury suppresses fibrinolysis following hemorrhagic shock in non-human primates (rhesus macaque).

Background: Hypoperfusion is associated with hyperfibrinolysis and early death from exsanguination, while tissue trauma is associated with hypofibrinolysis and delayed death from organ failure. We sought to elucidate the effects of injury patterns on fibrinolysis phenotypes using a non-human primate (NHP) model. Methods: NHPs were randomized to three injury groups (n=8/group): 60 min severe pressure-targeted controlled hemorrhagic shock (HS); HS + soft tissue injury (HS+); or HS + soft tissue injury + femur fracture (HS++). Animals were resuscitated and monitored for 360 min. Blood samples were collected at baseline (BSLN), end-of-shock (EOS), end-of-resuscitation (EOR), and T=360 min for assessments of: severity of shock (lactate) and coagulation via prothrombin time (PT), partial thromboplastin time (PTT), D-dimer, fibrinogen, anti-thrombin-III (AT-III), von Willebrand factor (vWF); and viscoelastic testing (ROTEM(R)). Results are reported as mean+/-SEM; statistics: two-way ANOVA and t-tests; significance: p

from Emergency Medicine via xlomafota13 on Inoreader http://ift.tt/2kus661