Resuscitation with Hextend((R)) decreases endogenous circulating heparin activity and accelerates clot initiation after hemorrhage in the rabbit

Hemorrhagic shock can result in a hypercoagulable state and has been associ ated with both hemorrhagic and thrombotic complications in the perioperativ e period. The author hypothesized that hemorrhage and resuscitation could r esult in a hypercoagulable state via changes in the heparin-antithrombin II I anticoagulant mechanism in rabbits. Rabbits sedated with ketamine underwe nt sham operation (n = 8) or hemorrhage (25 mL/kg blood shed) for 60 min, f ollowed by resuscitation with an equal volume of 5% human albumin (n = 8) o r Hextend (R) (n = 8). Coagulation analysis with the Thrombelastograph (R) analyzer and determination of endogenous heparin and antithrombin III activ ity were performed on arterial blood samples obtained before hemorrhage and 30 min after resuscitation. The reaction time significantly decreased by 3 4% after hemorrhage and resuscitation with Hextend (R), whereas no other si gnificant changes in Thrombelastograph (R) variables were noted. Antithromb in III activity was significantly less in the Albumin (83% +/- 8% of contro l, mean +/- SD) and Hextend (R) (88% +/- 8%) Resuscitated groups compared w ith the Sham-Operated animals. Of interest, only the Hextend (R) -Resuscita ted animals demonstrated a significant decrease in heparin activity (53.4 /- 13.6 mU/mL before hemorrhage, 42.3 +/- 5.6 mU/mL after resuscitation). A Hextende (R) -mediated decrease of both heparin and antithrombin III activ ity may explain the acceleration of clot initiation compared with albumin a dministration after hemorrhage in the rabbit.